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First Aid Chs Part 2 > Renal > Flashcards

Renal Flashcards

1
Q

What is the peritoneal state of the kidneys?

A

Primary retroperitoneal (never had a mesentery)

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2
Q

What is the peritoneal state of the ureter?

A

Primary retroperitoneal (never had a mesentery)

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3
Q

The adrenal medulla is derived from…

A

Neural crest

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4
Q

What vessels do the superior, middle, and inferior suprarenal arteries come off?

A

Superior - inferior phrenic artery; Middle - aorta artery; Inferior - Renal artery

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5
Q

What vein does the right suprarenal vein drain into?

A

IVC

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6
Q

What vein does the left suprarenal vein drain into?

A

L renal vein.

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7
Q

The pronephros becomes…

A

Nothing (regresses)

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8
Q

The mesonephros becomes…

A

Mesonephric (Wolffian) duct, which forms the ureteric bud, and becomes the male reproductive tract.

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9
Q

The metanephros becomes..

A

The permanent kidney, ascending from the sacral region into the upper lumbar region.

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10
Q

What (embryologically) forms the ureter?

A

The ureteric bud (from the caudal end of the mesonephros)

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11
Q

What (embryologically) forms the nephrons of the adult kidney?

A

Metanephric mesoderm (up to DCT); Ureteric bud (collecting duct)

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12
Q

What (embryologically) forms the urinary bladder?

A

The upper end of the urogenital sinus.

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13
Q

The allantois becomes…

A

The urachus (a fibrous cord).

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14
Q

The ureteric bud becomes…

A

The ureter, pelvis, calyces, and collecting ducts.

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15
Q

What is Hartnup’s disease?

A

Deficiency in neutral amino acid (tryptophan) transporter. Results in pellagra (niacin deficiency).

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16
Q

What artery does a horseshoe kidney get blocked by?

A

Inferior mesenteric a.

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17
Q

What is the cause of death in Potter syndrome?

A

Lung hypoplasia

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18
Q

What is Potter syndrome?

A

Oligohydramnios seen in bilateral renal agenesis or ARPKD. Results in: Lung hypoplasia (the cause of death in Potter syndrome); Flat face, low set ears, and extremity defects (result of compression of fetus due to oligohydramnios).

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19
Q

What is multicystic dysplastic kidney?

A

A NON-INHERITED, congenital malformation of renal parenchyma characterized by cysts and abnormal tissue (e.g. cartilage). Be able to differentiate this from ARPKD.

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20
Q

What will be seen in the liver in a patient with ARPKD?

A

Congenital hepatic fibrosis and hepatic cysts (think about this in a baby with portal HTN).

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21
Q

What are some other disorders seen in patients with ADPKD?

A

Berry aneurysms, hepatic cysts, MVP.

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22
Q

What is a major cause of sudden death in patients with ADPKD?

A

Rupture of berry aneurysms (SAH).

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23
Q

What will be the gross appearance of the kidneys in a patient with medullary cystic kidney disease?

A

Shrunken kidneys (vs. enlarged cystic kidneys with ADPKD or ARPKD).

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24
Q

What is the mechanism of inheritance of medullary cystic kidney disease?

A

AD

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25
Q

Where are the cysts located in medullary cystic kidney disease?

A

Medullary collecting ducts

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26
Q

What are the 3 subtypes of acute renal failure?

A

Prerenal, intrarenal, postrenal.

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27
Q

What is the BUN/Cr ratio in prerenal azotemia?

A

> 20

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28
Q

Why does the BUN/Cr ratio rise above 20 in prerenal azotemia?

A

Decreased blood flow to the kidney causes eventual release of aldosterone, which increases resorption of water. BUN is reabsorbed with water, raising the BUN in the blood. Creatinine is not reabsorbed, so the ratio increases.

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29
Q

What is the FENa in prerenal azotemia?

A

<1% (normal), because tubules are still intact and resorbing sodium well.

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30
Q

Why is the FENa <1% in prerenal azotemia?

A

Because the tubules are not damaged, so they are resorbing sodium regularly.

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31
Q

What will urine osmolality be in prerenal azotemia?

A

> 500 (tubules can still concentrate urine well).

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32
Q

What causes postrenal azotemia?

A

Obstruction downstream from the kidney.

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33
Q

What increases the BUN/Cr ratio in early postrenal azotemia?

A

Back pressure forcing BUN back into the blood. Creatinine is NOT reabsorbed, so the ratio increases.

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34
Q

What is the BUN/Cr ratio in long-standing postrenal azotemia?

A

15 in early postrenal azotemia, but eventually, the tubules are damaged, resulting in decreased reabsorption of BUN and a decreased BUN/Cr ratio).

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35
Q

What is the BUN/Cr ratio in early postrenal azotemia?

A

> 15 (back pressure forces BUN back into the blood. Creatinine is not reabsorbed, so the ratio increases).

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36
Q

What decreases the BUN/Cr ratio in long-standing postrenal azotemia?

A

Damage to the tubules with long standing postrenal azotemia results in impaired resorption of BUN, whose absorption was increased in early postrenal azotemia because of back pressure.

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37
Q

What is the FENAa in long standing postrenal azotemia?

A

> 2%, because the tubules are damaged and sodium can’t be effectively reabsorbed.

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38
Q

What will urine osmolality be in long standing postrenal azotemia?

A

t concentrate urine)

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39
Q

What is the most common cause of acute renal failure?

A

ATN (intrarenal azotemia)

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40
Q

What is the molecular cause of ATN?

A

Injury and necrosis of tubular epithelial cells plugs tubules, obstruction decreases GFR

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41
Q

What decreases the GFR in ATN?

A

Necrosis of cells plugging the tubules

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42
Q

What is seen in the urine in ATN?

A

Brown granular (“muddy”) casts.

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43
Q

What is the BUN/Cr ratio in ATN (intrarenal azotemia)?

A

< 15 (damaged tubules, can’t reabsorb BUN)

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44
Q

What is the FENa in ATN (intrarenal azotemia)?

A

> 2% (damaged tubules, can’t reabsorb sodium)

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45
Q

What is urine osmolality in ATN (intrarenal azotemia)?

A

t concentrate urine)

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46
Q

What are the two major etiologies of ATN?

A

Ischemia, nephrotoxins.

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47
Q

What part of the nephron is particularly susceptible to toxic ATN?

A

PCT (getting the highest concentration of drugs)

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48
Q

What two parts of the nephron are particularly susceptible to ischemic ATN?

A

PCT and TALOH

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49
Q

What antimicrobial family can cause ATN?

A

Aminoglycosides

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50
Q

What are some causes of toxic ATN?

A

Aminoglycosides, heavy metals, myoglobinuria, ethylene glycol, radiocontrast dye, urate (tumor lysis syndrome).

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51
Q

What is tumor lysis syndrome and what can be done to decrease the risk of it?

A

Rapid killing of leukemia cells causes release of purines, which are metabolized into uric acid, which can cause ATN. To decrease the risk, hydrate the patient well or give allopurinol.

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52
Q

What are the 3 phases of ATN?

A
  1. Inciting event 2. Maintenance - oliguria (death most commonly occurs here!), risk of hyperkalemia. 3. Recovery phase - polyuric - BUN and Creatinine fall, risk of hypokalemia.
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53
Q

In which phase of ATN does death most commonly occur?

A

Oliguric (maintenance) phase due to hyperkalemia.

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54
Q

What is acute interstitial nephritis and what causes it?

A

Drug induced HSR of interstitium and tubules resulting in intrarenal ARF. Causes include NSAIDS, PCN, diuretics. Results in eosinophils in the urine. Resolves with cessation of drug, but can progress to renal papillary necrosis.

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55
Q

What will be seen on biopsy in acute interstitial nephritis?

A

Acute inflammatory infiltrate in CT between tubules. Tubules are spared.

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56
Q

What is seen in the urine in a patient with acute interstitial nephritis?

A

Eosinophils

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57
Q

Patient on NSAIDs presents with eosinophils in urine. Dx?

A

Acute interstitial nephritis (drug induced HSR to drug).

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58
Q

Chronic use of which two drugs can cause renal papillary necrosis?

A

Phenacetin, aspirin.

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59
Q

What are some causes of renal papillary necrosis?

A

Chronic analgesic abuse (phenacetin or aspirin), DM, sickle cell, pyelonephritis.

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60
Q

A patient abusing analgesics over a long period of time is at risk for which renal disorder?

A

Renal papillary necrosis.

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61
Q

What is the hallmark of nephrotic syndrome?

A

Proteinuria > 3.5 g/day

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62
Q

What happens to serum albumin in nephrotic syndrome?

A

Decreases (lost in protein - proteinuria >3.5 g/day), results in edema.

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63
Q

Why do patients with nephrotic syndrome become hypercoagulable?

A

Lose antithrombin III

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64
Q

What happens to cholesterol and lipid levels in a patient with nephrotic syndrome?

A

The patient becomes hypercholesterolemic and hyperlipidemic.

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65
Q

What is the most common cause of nephrotic syndrome in kids?

A

Minimal change disease

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66
Q

Minimal change disease is associated with what neoplasm?

A

Hodgkin’s disease

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67
Q

What 3 things form the filtration barrier into the tubular space?

A

Endothelial cells, which sit on a basement membrane, which sits on podocytes (epithelial cells).

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68
Q

What is lost in minimal change disease?

A

Podocyte foot processes

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69
Q

What causes foot process effacement in minimal change disease?

A

Cytokines (which are massively overproduced in Hodgkin’s disease, which is why patients with HL get MCD).

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70
Q

What is seen on H&E in minimal change disease?

A

Normal glomeruli

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71
Q

What is seen on EM in minimal change disease?

A

Effacement (flattening) of foot processes.

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72
Q

What protein is decreased in serum in minimal change disease?

A

Only albumin (not immunoglobulin).

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73
Q

What is the treatment for minimal change disease?

A

Corticosteroids (because damage is mediated by cytokines from T cells).

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74
Q

Does minimal change disease cause nephrotic or nephritic syndrome?

A

Nephrotic

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75
Q

Does focal segmental glomerulosclerosis cause nephrotic or nephritic syndrome?

A

Nephrotic

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76
Q

What is the most common cause of nephrotic syndrome in Hispanics and African Americans?

A

Focal segmental glomerulosclerosis (this is what Alonzo Mourning had)

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77
Q

A patient with sickle cell disease develops nephrotic syndrome. Dx?

A

Focal segmental glomerulosclerosis

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78
Q

A patient with HIV develops nephrotic syndrome. Dx?

A

Focal segmental glomerulosclerosis

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79
Q

A heroin addict develops nephrotic syndrome. Dx?

A

Focal segmental glomerulosclerosis

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80
Q

What is seen on H&E in focal segmental glomerulosclerosis?

A

Focal (not all glomeruli affected) and segmental (only part of the glomerulus affected) sclerosis (dark pink color).

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81
Q

A patient not responding to steroids in minimal change disease will progress to…

A

Focal segmental glomerulosclerosis

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82
Q

What will be seen on EM in focal segmental glomerulosclerosis?

A

Effacement of foot processes (just like MCD - patients who don’t respond to steroids in MCD progress to FSGS).

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83
Q

Does membranous nephropathy give nephrotic or nephritic syndrome?

A

Nephrotic

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84
Q

What is the most common cause of nephrotic syndrome in Caucasian adults?

A

Membranous nephropathy

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85
Q

A patient with HBV develops nephrotic syndrome. Dx?

A

Membranous nephropathy most common, MPGN type I next most common.

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86
Q

A patient with SLE develops nephrotic syndrome. Dx?

A

Membranous nephropathy

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87
Q

A patient with HCV develops nephrotic syndrome. Dx?

A

Membranous nephropathy most common, type I MPGN next most common.

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88
Q

A patient with a solid cancer develops nephrotic syndrome. Dx?

A

Membranous nephropathy

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89
Q

What is seen on H&E in membranous nephropathy?

A

Thick glomerular basement membrane

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90
Q

What causes thickening of the basement membrane in membranous nephropathy?

A

Immune complex deposition

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91
Q

What is seen on EM in membranous nephropathy?

A

Subepithelial deposits with “spike and dome” appearance.

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92
Q

Subepithelial deposits with “spike and dome” appearance on EM

A

Membranous nephropathy (generate a “dome” of new BM over immune complex deposits with spikes between the domes).

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93
Q

What is seen on immunofluorescence in membranous nephropathy?

A

Granular appearance (due to immune complex deposition).

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94
Q

Anytime you see the word “membranous”, in nephrotic syndrome, what is the underlying cause?

A

Immune complex deposition.

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95
Q

Does membranoproliferative glomerulonephritis cause nephrotic or nephritic syndrome?

A

Nephritic, nephrotic, or both

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96
Q

What causes the “tram track” appearance in membranoproliferative glomerulonephritis?

A

Mesangial cell proliferation cutting the glomerular BM in half, causing separation of the membrane.

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97
Q

Tram track appearance of GBM.

A

Membranoproliferative glomerulonephritis

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98
Q

What causes membranoproliferative glomerulonephritis?

A

Immune complex deposition

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99
Q

What is seen on immunofluorescence in membranoproliferative glomerulonephritis?

A

Granular appearance (immune complex deposition).

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100
Q

What are the two types of membranoproliferative glomerulonephritis?

A

Type I - subendothelial deposition, associated with HBV/HCV. Type II - intramembranous deposition, associated with C3 nephritic factor.

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101
Q

Where are the deposits in type I membranoproliferative glomerulonephritis?

A

Between the endothelium and the basement membrane (subendothelial).

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102
Q

Where are the deposits in type II membranoproliferative glomerulonephritis?

A

Within the basement membrane (intramembranous)

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103
Q

What infections are associated with type I membranoproliferative glomerulonephritis?

A

HBV/HCV

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104
Q

What is C3 nephritic factor?

A

Autoantibody that prevents the breakdown of C3 convertase, which drives complement, causing intramembranous immune depositions, which cause type II membranoproliferative glomerulonephritis.

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105
Q

C3 nephritic factor is associated with which disorder?

A

Type II membranoproliferative glomerulonephritis

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106
Q

Intramembranous complex deposits…

A

Type II membranoproliferative glomerulonephritis

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107
Q

Subendothelial complex deposits…

A

Type I membranoproliferative glomerulonephritis

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108
Q

Which subset of MPGN is more likely to cause the “tram track” appearance?

A

Type I (subendothelial depositions)

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109
Q

Diabetic nephropathy causes nephritic or nephrotic syndrome?

A

Nephrotic

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110
Q

What is the molecular etiology of diabetic nephropathy?

A

High serum glucose causing non-enzymatic glycosylation of vascular basement membranes resulting in hyaline arteriolosclerosis.

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111
Q

Which arteriole is preferentially damaged in diabetic nephropathy and what does damage of this arteriole cause?

A

Efferent arteriole damage (this is why ACE inhibitors are good in diabetics!!), causing backup of pressure in glomerulus and hyperfiltration, which leads to sclerosis of the mesangium of the glomerulus.

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112
Q

What is the first change in the kidney of a diabetic patient?

A

Non-enzymatic glycosylation of vascular basement membrane.

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113
Q

What is the hallmark of diabetic glomerulopathy?

A

Sclerosis of the mesangium and formation of Kimmelsteil-Wilson nodules

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114
Q

What are Kimmelsteil-Wilson nodules?

A

Dense nodular sclerosis of the mesangium seen in diabetic glomerulopathy.

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115
Q

Does systemic amyloidosis cause nephritic or nephrotic syndrome?

A

Nephrotic

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116
Q

How does amyloidosis cause nephrotic syndrome?

A

Deposits in the mesangium

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117
Q

Name the 6 glomerulopathies that cause nephrotic syndrome.

A

Minimal change disease; Focal segmental glomerulosclerosis; Diabetic glomerulopathy; Systemic amyloidosis; Membranous nephropathy; Membranoproliferative glomerulonephritis

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118
Q

What is the hallmark of nephritic syndrome?

A

Glomerular inflammation and bleeding

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119
Q

Quantify the proteinuria seen in nephritic syndrome.

A

<3.5 g/day

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120
Q

RBC casts are seen in nephrotic or nephritic syndrome?

A

Nephritic

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121
Q

What is the function of C5a?

A

Neutrophil chemotaxis

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122
Q

What virulence factor in strep pyogenes increases risk for PSGN?

A

M protein

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123
Q

How long after infection does PSGN occur?

A

2-3 weeks

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124
Q

Hypertension, salt retention, and periorbital edema are seen with nephritic or nephrotic syndrome?

A

Nephritic

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125
Q

What is seen on H&E in post-strep glomerulonephritis?

A

Hypercellular, inflamed glomerulus

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126
Q

What is seen on immunofluorescence in post-strep glomerulonephritis?

A

Granular appearance

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127
Q

What is seen on electron microscopy in post-strep glomerulonephritis?

A

Subepithelial “humps”

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128
Q

What is seen on H&E in rapidly progressive glomerulonephritis?

A

Crescents in Bowman’s space

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129
Q

What composes the crescents seen in rapidly progressive glomerulonephritis?

A

Fibrin and macrophages

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130
Q

What is seen on immunofluorescence in Goodpasture’s syndrome?

A

Linear immunofluorscence

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131
Q

Antibodies in Goodpasture’s syndrome are targeted against…

A

Type IV collagen in glomerular (hematuria) and alveolar (hemoptysis) basement membranes

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132
Q

What is seen on immunofluorescence in diffuse proliferative glomerulonephritis?

A

Granular appearance

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133
Q

Where are the deposits seen in diffuse proliferative glomerulonephritis?

A

Subendothelial

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134
Q

What is the most common renal disease seen in SLE?

A

Diffuse proliferative glomerulonephritis

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135
Q

What is seen on renal immunofluorescence in Wegener’s granulomatosis?

A

Nothing (pauci-immune)

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136
Q

What is seen on renal immunofluorescence in microscopic polyangiitis?

A

Nothing (pauci-immune)

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137
Q

What is seen on renal immunofluorescence in Churg-Strauss syndrome?

A

Nothing (pauci-immune)

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138
Q

List 3 causes of pauci-immune glomerulonephritis.

A

Churg-Strauss syndrome, microscopic polyangiitis, Wegener’s granulomatosis. All are negative on immunofluorescence and should be worked up with an ANCA test.

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139
Q

Where does the p-ANCA antibody bind and which two causes of nephritic disease is it seen in?

A

Binds near the nucleus of the neutrophil (perineuclear). Seen in Microscopic polyangiitis and Churg-Strauss syndrome.

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140
Q

Where does the c -ANCA antibody bind and what nephritic disease is it seen in?

A

Binds in the cytoplasm of the neutrophil. Seen in Wegener’s granulomatosis.

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141
Q

What 3 things bleed in Wegner’s granulomatosis?

A

Nasal passages, lungs, kidneys (hematuria)

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142
Q

What 3 things are seen in Churg-Strauss syndrome that aren’t seen in microscopic polyangiitis?

A

Granulomatous inflammation, Eosinophilia, Asthma (Both are p-ANCA positive)

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143
Q

What is seen on H&E in diffuse proliferative glomerulonephritis?

A

Wire looping of capillaries

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144
Q

What deposits in Berger disease, and where does it deposit?

A

IgA deposits (it is also called IgA nephropathy) in the mesangium of the glomeruli.

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145
Q

IgA nephropathy (Berger disease) typically follows…

A

A viral mucosal infection. End up producing excess IgA to fight the infection, which ends up depositing in the mesangium.

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146
Q

What is the common presentation and age group of IgA nephropathy (Berger disease)?

A

Episodic gross or microscopic hematuria with RBC casts usually following a mucosal infection. Seen in kids.

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147
Q

Production of what is decreased in Alport syndrome?

A

Type IV collagen

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148
Q

What is the method of transmission of Alport syndrome?

A

X-linked (85% dominant)

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149
Q

What happens to the basement membrane in Alport syndrome?

A

It is split due to a mutation in type IV collagen.

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150
Q

What are the 3 key findings in Alport syndrome?

A

Isolated hematuria, sensory hearing loss, visual disturbances.

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151
Q

Is Alport syndrome nephrotic or nephritic?

A

Nephritic.

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152
Q

List 6 causes of nephritic syndrome.

A

Acute post-streptococcal glomerulonephritis; Rapidly progressive glomerulonephritis (Wegener’s, Goodpasture’s, Microscopic polyangiitis, Churg-Strauss); Diffuse proliferative glomerulonephritis; Berger disease ( IgA nephropathy); Alport syndrome; Membranoproliferative glomerulonephritis

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153
Q

A patient with Henoch-Schoenlein purpura is at increased risk of developing what renal disorder?

A

IgA nephropathy (Berger disease)

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154
Q

What is seen on urine dipstick in cystitis?

A

Positive leukocyte esterase (due to leukocytes in urine); Nitrites (bacteria convert nitrates in urine into nitrites)

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155
Q

What is the #1 cause of cystitis?

A

E. coli

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156
Q

What is the #1 cause of cystitis in young sexually active women?

A

S. saprophyticus

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157
Q

Sterile pyuria is suggestive of…

A

Urethritis due to C. trachomatis or N. gonorrhoeae

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158
Q

What are the signs and symptoms of pyelonephritis?

A

Fever, flank pain, WBC casts, leukocytosis in addition to symptoms of cystitis (which has no systemic symptoms).

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159
Q

What is the #1 cause of acute pyelonephritis?

A

E. coli

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160
Q

Describe the appearance of the kidney in chronic pyelonephritis.

A

Cortical scarring with blunted calyces.

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161
Q

Scarring at the upper and lower poles of the kidneys is characteristic of…

A

Vesicoureteral reflux

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162
Q

What is “thyroidization” of the kidney and with what disease is it associated?

A

Plugging of the renal tubules with eosinophilic casts looks like thyroid tissue microscopically. This is seen in chronic pyelonephritis.

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163
Q

What type of renal stones are the most common?

A

Calcium stones (oxalate, phosphate)

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164
Q

What are the only renal stones that are radiolucent on x-ray?

A

Uric acid is radiolUscent

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165
Q

What causes ammonium magnesium phosphate stones?

A

Infection with proteus vulgaris or klebsiella species, which cause alkaline environment that leads to formation of the stone.

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166
Q

What type of renal stones are typically “staghorn”?

A

Ammonium magnesium phosphate stones (“struvite” or “triple”)

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167
Q

Leukemia increases the risk for which type of renal stones?

A

Uric acid (due to increased cell turnover).

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168
Q

How are uric acid stones treated?

A

Alkalinization of urine (potassium bicarbonate) and hydration, allopurinol in patients with gout.

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169
Q

If you see a staghorn calculus in a child, what disorder should you think about?

A

Cystinuria (staghorne calculi are commonly cysteine in kids, struvite in adults).

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170
Q

How do you treat someone with cysteine stones?

A

Alkalinization of urine, hydration.

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171
Q

Why does renal failure cause anemia?

A

Reduced EPO

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172
Q

What cells in the kidney produce EPO?

A

Renal peritubular interstitial cells

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173
Q

Why do patients in renal failure develop hypocalcemia?

A
  1. Can’t excrete phosphate. Increased phosphate binds calcium in the blood. 2. Can’t 1-alpha hydroxylate vitamin D (results in osteomalacia).
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174
Q

What is osteitis fibrosa cystica and why does it happen in renal failure?

A

High PTH due to hypocalcemia in renal failure causes resorption of calcium from the bone, which eventually causes fibrosis and cyst formation.

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175
Q

Patients on dialysis are at an increased risk for what cancer?

A

Renal cell carcinoma (secondary to shrunken kidneys that develop cysts in dialysis).

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176
Q

Tuberous sclerosis increases the risk for what renal neoplasm?

A

Angiomyolipoma (blood vessel, muscle, fat hamartoma)

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177
Q

Renal cell carcinoma arises from..

A

PCT cells

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178
Q

What is the triad of symptoms seen in renal cell carcinoma?

A

Hematuria, palpable mass, flank pain

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179
Q

List 4 potential paraneoplastic syndromes caused by renal cell carcinoma.

A

EPO - polycythemia; Renin - HTN; PTHrP - hypercalcemia; ACTH - Cushing syndrome

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180
Q

How does renal cell carcinoma cause a varicocele?

A

Invasion of the left renal vein blocks the L testicular vein

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181
Q

Explain the appearance of renal cell carcinoma on H&E.

A

Polygonal cells with clear cytoplasm - “clear cell”.

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182
Q

Through which channels does renal cell carcinoma spread?

A

Veins

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183
Q

Pathogenesis of renal cell carcinoma involves loss of which tumor suppressor gene?

A

VHL (increases IGF-1 and HIF transcription factor which increases VEGF and PDGF).

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184
Q

How is Von Hippel-Lindau disease transmitted?

A

Autosomal dominant

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185
Q

Von Hippel-Lindau disease increases the risk for which two neoplasms?

A

Hemangioblastoma of the cerebellum and renal cell carcinoma.

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186
Q

What is the #1 renal tumor in children?

A

Wilms tumor

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187
Q

What is seen on biopsy of Wilms tumor?

A

Embryonic glomerular and tubular structures (blastema is the key component)

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188
Q

What is the classic presentation of Wilms tumor?

A

Large, unilateral flank mass with hematuria and hypertension (secondary to renin secretion).

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189
Q

What is the genetic component of Wilms tumor?

A

Deletion of tumor suppressor gene WT1 on chromosome 11. This is especially seen in WAGR syndrome and Beckwith-Widemann syndrome.

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190
Q

What is WAGR syndrome?

A

Wilms tumor; Aniridia; Genital anomalies; Developmental delay; seen with deletion of tumor suppressor gene WT1 on chromosone 11

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191
Q

What is Beckwith-Widemann Syndrome?

A

Wilms tumor; Neonatal hypoglycemia; Muscular hemyhypertrophy; Organomegaly (tongue); Seen with deletion of tumor suppressor gene WT1 on chromosome 11

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192
Q

What is the #1 risk factor for transitional cell carcinoma of the bladder?

A

Smoking (other risks are naphthylamine, azo dyes, and long term cyclophosphamide or phenacetin).

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193
Q

What is the general presentation of urothelial carcinoma?

A

Painless hematuria

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194
Q

What are the two pathways through which urothelial carcinoma can arise?

A

Flat - urothelial carcinoma that starts as high grade and invades. Associated with early p53 mutations. Papillary- starts as low grade, progresses to high grade, and invades.

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195
Q

p53 mutations are associated with what subtype of urothelial carcinoma?

A

Flat (starts as high grade, invades)

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196
Q

Schistosoma hematobium increases the risk for what cancer?

A

Squamous cell carcinoma of the bladder (boards will present this in a young, Middle-Eastern male with bladder CA)

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197
Q

In order to have squamous cell carcinoma of the bladder, there first must be…

A

Squamous cell metaplasia of the bladder

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198
Q

List 3 risk factors for squamous cell cancer of the bladder.

A

Chronic cystitis; S. hematobium; Long standing nephrolithiasis

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199
Q

Exstrophy of the bladder increases the risk for which type of cancer?

A

Adenocarcinoma of the bladder

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200
Q

Urachal remnant increases the risk for which type of cancer?

A

Adenocarcinoma of the dome of the bladder

201
Q

What is the urachus and what is its function?

A

A tube that connects the fetal bladder to the yolk sac, allowing the bladder to drain in the yolk sac.

202
Q

A patient presents with adenocarcinoma of the dome of the bladder (most superior portion). What most likely caused this?

A

Persistent urachus

203
Q

What is cystitis glandularis and what does it increase the risk for?

A

Chronic inflammation of the bladder leading to columnar metaplasia, which can lead to adenocarcinoma of the bladder.

204
Q

What is hydronephrosis?

A

Backup of urine into the kidney - can be caused by obstruction or vesicoureteral reflux and leads to parenchymal thinning in chronic cases.

205
Q

What is the #1 risk factor in the oliguric (maintenance) phase of ATN?

A

Hyperkalemia

206
Q

What is the #1 risk factor in the recovery phase of ATN?

A

Hypokalemia (patient is polyuric).

207
Q

What is a renal oncocytoma?

A

Rare tumor that arises from collecting duct cells.

208
Q

What serum protein will be reduced in patients with post-strep glomerulonephritis?

A

C3

209
Q

What is the appearance of the glomerulus on H&E in a patient with post-strep GN?

A

Hypercellular with “lumpy bumpy” appearance.

210
Q

What two things are deposited on the renal BM in Goodpasture syndrome?

A

C3 and IgG

211
Q

What causes the cells to appear clear in renal cell carcinoma?

A

Glycogen and lipid accumulation

212
Q

What three things are deposited on the BM in post-strep GN?

A

!gG, IgM, and C3.

213
Q

What is the most important prognostic factor in patients with post-strep GN?

A

Age (kids much more likely to resolve)

214
Q

What autoantibody is present in patients with idiopathic membranous glomerulopathy?

A

IgG to phospholipase A2 receptor (PLA2R)

215
Q

What needs to be seen on urine culture in order to make a diagnosis of a UTI?

A

Greater than 100,000 colony forming units per mL

216
Q

What does leukocyte esterase in a UTI mean?

A

UTI is bacterial

217
Q

What do nitrites in urine mean in a UTI?

A

The bacteria is gram negative

218
Q

What are the 3 drugs that can be given for acute, uncomplicated UTI?

A

TMP/SMX, nitrofurantoin, fosfomycin

219
Q

What is the MOA of nitrofurantoin?

A

Reduced by bacterial flaviproteins to reactive intermediates, which inactivate many different bacterial processes.

220
Q

Sulfamethoxazole inhibits…

A

Bacterial dihydropterate synthetase (Mimics PABA)

221
Q

Trimethoprim inhibits…

A

Bacterial DHFR

222
Q

What is the MOA of fosfomycin?

A

Inhibits production of murein monomers by binding to active site of cytoplasmic enolpyrivate transferase and preventing the addition of PEP to UDP-NAG (first step in cell wall synthesis).

223
Q

What are the three first line drugs for acute pyelonephritis?

A

Ciprofloxacin, levofloxacin, TMP/SMX

224
Q

In what patient group should asymptomatic bacteriuria be treated?

A

Pregnant women

225
Q

Which UTI drugs are safe in pregnancy?

A

Fosfomycin, nitrofurantoin

226
Q

TMP/SMX in pregnancy can have what effect on the fetus?

A

Kernicterus

227
Q

What is the first line drug for acute pyelonephritis in a pregnant woman?

A

3rd generation beta lactam (ceftriaxone).

228
Q

What does the sodium-cyanide/nitroprusside test test for?

A

Cystinuria - seen in young males with recurrent stones.

229
Q

Hexagonal shaped crystals in urine

A

Cysteine stone

230
Q

Envelope shaped crystals in urine

A

Calcium oxalate crystals - ethylene glycol poisoning.

231
Q

<p>WBC casts + symptoms of cystitis is pathogonomic for...</p>

A

<p>Acute pylelonephritis</p>

232
Q

What are the three embryological forms of the kidney?

A

Pronephros - Week 4 then degenerates
Mesonephros - interim kidney for first trimester, later contributes tot he male genital system
Metanephros - permanent - appears in 5th week of gestation

233
Q

What is the ureteric bud?

A

Derived from caudal end of mesonephros; gives rise to ureter, pelvises, calyces, and collecting ducts
fully canalized by 10th week

Induces the metanephros to differentiate into the renal tubular epithelial structures

234
Q

What is the Metanephric mesenchyme?

A

Ureteric bud induces this tissue to form the glomerulus through the distal convoluted tubules

235
Q

What is the significance of the ureteropelvic junction?

A

Last to canalize - most common site of obstruction (hydronephrosis) in the fetus

236
Q

What is the mnemonic for Potter’s syndrome?

A 
POTTER
Pulmonary hypoplasia (cause of death)
Oligohydraminos
Twisted skin (wrinkled)
Twisted face (facial deformities)
Extremities (limb deformities)
Renal agenesis
237
Q

What type of infants commonly develop Potter’s syndrome?

A

ARPKD, posterior urethral valves, bilateral renal agenesis

238
Q

What part of the kidneys fuse in a horeshoe kidney?

A

Inferior poles of the kidneys

note that the kidney functions normally

239
Q

What type of patient do you often see with a horeshoe kidney?

A

Turner syndrome

240
Q

What causes multicystic dysplastic kidney?

A

Abnormal interaction between the ureteric bud and metanephric mesenchyme

241
Q

What are the findings in multicystic dysplastic kidney?

A 
Leads to a nonfunctional kidney consisting of cysts and connective tissue. 
If unilateral (most common) generally asymptomatic with compensatory hypertrophy of contralateral kidney
- often diagnosed prenatally via ultrasound
242
Q

What are the 3 things that tell the juxtaglomerular cells to release renin?

A
  1. beta-1 adrenergic stimuli (increased sympathetics)
  2. Low sodium in the distal convoluted tubule (sensed via macula densa)
  3. Low pressure in afferent arterioles of glomerulus
243
Q

What is the function of the juxtaglomerular cells? of the macula densa?

A

Juxtaglomerular cells: secrete renin and monitor BP

Macula densa cells: senses sodium levels

244
Q

Which part of the kidney contains the glomeruli and which part contains the nephrons?

A

Cortex contains the glomeruli

Medulla contains the nephrons

245
Q

What is the significance of the location of the ureters and arteries?

A

Ureters pass under the uterine artery and under the ductus deferens (retroperitoneal)

246
Q

How much of the total body weight is total body water?

A

60%

247
Q

How much of the total body water is:

  • extracellular fluid
  • intracellular fluid
  • plasma volume
  • interstitial volume
A

Total body water is 60% of total body weight
Extracellular fluid is 1/3 of total body water
intracellular fluid is 2/3 of total body water
plasma volume is 1/4 of extracellular fluid
interstitial volume is 3/4 of extracellular fluid

248
Q

What is the 60 - 40 -20 rule?

A

60% total body water
40% ICF
20% ECF

249
Q

How is plasma volume measured?

A

by radiolabeled albumin

250
Q

How is extracellular volume measured?

A

by inulin

251
Q

What 3 things make of the glomerular filtration barrier?

A
  1. fenestrated capillary endothelium (size barrier)
  2. Fused basement membrane with heparin sulfate (negative charge barrier)
  3. Epithelial layer consisting of podocyte foot processes
252
Q

What happens with a loss of the charge barrier in the glomerular filtration barrier?

A

The charge barrier is lost in nephrotic syndrome which leads to albuminuria. hypoproteinemia, generalized edema and hyperlipidemia

253
Q

What is the formula for renal clearance?

A 
Clearance = (Urine concentration x urine flow rate) / Plasma concentration
C = UV/P
254
Q

What are the there possibilities with Renal clearance?

A

Cx < GFR = net tubular reabsorption of x
Cx > GFR = net tubular secretion of x
Cx = GFR = no net secretion or reabsorption (ie inulin)

255
Q

What can be used to calculate GFR?

A

Inulin can be used to calculate GFR because it is freely filtered and is neither reabsorped nor secreted

256
Q

What is the formula for GFR?

A

GFR = Uinulin x V / Pinulin = Cinulin

Note that creatinine clearance is an approximate measure of GFR - slightly overestimates GFR because it’s moderately secreted by renal tubules

257
Q

What is the oncotic pressure in bowman’s space normally?

A

0

258
Q

What is normal GFR?

A

~100 mL/min

259
Q

What is the formula for effective renal plasma flow?

A

Renal plasma flow = PAH clearance = Urine PAH x V/ P PAH

260
Q

What can be used to measure the effective renal plasma flow?

A

The clearance of PAH (para-amino hippuric acid) which is both filtered and actively secreted into the proximal tubule

261
Q

What is the formula for renal blood flow?

A

RBF = RPF/(1-hematocrit)

262
Q

What is the formula for filtration fraction?

A

Filtration Fraction = GFR of inulin / RPF of PAH

Filtration fraction is the portion of blood going to the kidney that’s filtered through the glomerulus

263
Q

What does dehydration cause?

A

way decreased renal plasma flow
decreased GFR
increased filtration fraction

264
Q

What is a normal filtration fraction?

A

20%

265
Q

What is a filtered load equation?

A

Filtered load = GFR x plasma concentration

266
Q

What effect do prostaglandins have on the afferent arteriole?

A

Prostaglandins dilate the afferent arteriole leading to increased RPF and increased GFR and a constant FF

note that NSAIDS will cause the exact opposite since they inhibit prostaglandins, they will lead to constriction at the afferent arteriole

267
Q

What effect does Angiotensin II have on the efferent arteriole?

A

Angiotensin II preferentially constricts the efferent arteriole leading to decreased RPF, increased GFR and therefore increased FF

Note that ACE inhibitors block angiotensin II and therefore will dilate the efferent arteriole having the opposite effect

268
Q

What are glomerular dynamics that will be seen with afferent arteriole constriction?

A

decreased RPF
decreased GFR
no change to FF

269
Q

What are glomerular dynamics that will be seen with Efferent arteriole constriction?

A

Decreased RPF
Increased GFR
Increased FF

270
Q

What are glomerular dynamics that will be seen with Increased plasma protein concentration?

A

No change in RPF
Decreased GFR
Decreased FF

Note that with increased serum protein you have increased osmotic pull so less blood will escape

271
Q

What are glomerular dynamics that will be seen with Decreased plasma protein concentration?

A

No change in RPF
Increased in GFR
Increased in FF

272
Q

What are glomerular dynamics that will be seen with constriction of the ureter?

A

No change in renal plasma flow
decreased GFR
decreased FF

273
Q

What are glomerular dynamics that will be seen with dilation of the afferent arteriole?

A

Increased RPF
Increased GFR
constant FF

274
Q

What is the formula for excretion rate?

A

U[x] x V = urinary concentration of x times the urine flow rate

275
Q

What is the formula for reabsorption?

A

Reabsorption = Filtered - excreted

276
Q

What is the formula for secretion?

A

Secretion = excreted - filtered

277
Q

What is normal glucose clearance?

A

Glucose at a normal plasma level is completely reabsorbed in the proximal tubule by Na+/glucose cotransport

278
Q

When do you start to see glucose in the urine?

A

At plasma glucose of ~ 160mg/dl, glucosuria begins (threshold)
At 350 mg/dL all transporters are full saturated (Tm)

279
Q

What happens in pregnancy with glucose and amino acids?

A

Normal pregnancy reduces reabsorption of glucose and amino acids in the proximal tubule leading to glucosuria and aminoaciduria

280
Q

What is Hartnup’s disease?

A

Deficiency of neutral aminoa acid (tryptophan) transporter - results in pellagra

No tryptophan = no niacin (Vit B3) = 3 D’s of pellagra = Dermatitis, diarrhea, dementia and maybe death

281
Q

Which part of the kidney uses isotonic absorpotion?

A

Early proximal tubule

282
Q

What does PTH do in the proximal tubule?

A

Inhibits Na/phosphate co transport leading to phosphate excretion

283
Q

What does Angiotensin II do in the proximal tubule?

A

Stimulates Na/H exchanger leading to increased sodium, water and bicarb reabsorption
This permits a contraction alkalosis

284
Q

What is the concentrating segment of the nephron?

A

Thin descending loop of henle

Makes urine hypertonic

285
Q

What solute is impermeable in the thin descending loop of henle?

A

Sodium!

The thin descending loop passively reabsorbs water via medullary hypertonicity and it is impermeable to sodium

286
Q

What portion of the kidney actively reabsorbs sodium, potassium and chloride?

A

Thick ascending loop of henle.

Indirectly induces the paracellular reabsorption of magnesium and calcium through positive lumen potential generated by potassium back lead

287
Q

What section of the nephron is impermeable to water?

A

Thick ascending loop of Henle.

This section makes the urine less concentrated as it ascends

288
Q

What portion of the nephron actively reabsorbs sodium and chloride and makes the urine hypotonic?

A

Early distal convoluted tubule

289
Q

What effect does PTH have at the early distal convoluted tubule?

A

Increased calcium/sodium exchange leading to increased calcium reabsorption

290
Q

What portion of the nephron is regulated by aldosterone and what are the effects?

A

Collecting tubules
aldosterone reabsorbs sodium in exchange for secreting potassium and hydrogen

  • Aldosteron acts on mineralocorticoid receptor leading to the insertion of sodium channels on the luminal side
291
Q

Where in the nephron does ADH have it’s effect and what does it do?

A

ADH works at the collecting tubule principal cell at the V2 receptor causing insertion of aquaporin water channels on the luminal side

292
Q

Why does tubular inulin increase in concentration (but not amount) along the proximal tubule?

A

As a result of water reabsorption

and inulin is neither reabsorbed or secreted

293
Q

What is the function of Angiotensin II on the vascular smooth muscle?

A

Angiotensin II acts at AT1 receptors on the vascular smooth muscle to cause vasoconstriction and an increased in BP

294
Q

What is the function of Angiotensin II on the efferent arteriole off the glomerulus?

A

Angiotensin II causes constriction of the efferent arteriole of the glomerulus leading to increased filtration fraction to preserve renal function (GFR) in low-volume states (like when RBF is decreased)

295
Q

What is the function of Angiotensin II on The adrenal gland?

A

Angiotensin II causes release of aldosterone.

  • Aldosterone increased sodium channel and Na/K pump insertion in principal cells in the kidney
  • This enhances K+ and H+ excretion (upregulates principal cell K+ channels and intercalated cell H+ channels)
  • This creates favorable Na+ gradient for Na and water reabsorption
296
Q

What is the function of Angiotensin II on the posterior pituitary?

A

Angiotensin II functions to increase ADH release from the posterior pituitary resulting in increased water channel insertion in principal cells leading to increased water reabsorption

297
Q

What is the function of Angiotensin II on the proximal tubule?

A

Angiotensin II increased proximal tubule Na/H activity leading to sodium, bicarb, and water reabsorption (permits contraction alkalosis)

298
Q

What is the function of Angiotensin II on the hypothalamus?

A

Stimulates hypothalamus leading to increased thirst

299
Q

What is the function of Angiotensin II on baroreceptors?

A

Angiotensin II affects baroreceptors function by limiting reflex bradycardia which would normally accompany it’s pressor effects - helps to maintain blood volume and blood pressure

300
Q

What is the function of ANP?

A

Released from the atria in response to increased volume

  • may act as a “check” on the R-A-A system
  • relaxes vascular smooth muscle via cGMP causing increased GFRP and decreased renin
301
Q

What is the function of ADH?

A

Primarily regulates osmolarity but also responds to low blood volume, which takes precedence over osmolarity

302
Q

What is the function of Aldosterone?

A

Primarily regulates blood volume, in low volume states both ADH and aldosterone act to protect blood volume

303
Q

What comprises the juxtaglomerular apparatus?

A
  • JG cells (modified smooth muscle of afferent arteriole)

- macula densa (NaCl sensor, part of the distal convoluted tubule

304
Q

Can beta blockers decrease renin release?

A

Beta blockers can decrease BP by inhibits Beta 1 receptors of the JGA causing decreased renin release

305
Q

What is Erythropoietin?

A

released by interstitial cells in the peritubular capillary bed in response to hypoxia

306
Q

How does the kidney increase vitamin D levels?

A

PTH acts on the kidney to increase 1 alpha hydroxylase in the kidney which causes the proximal tubule cells to convert 25-OH vitamin D to 1,25 OH2 vitamin D (active form)

307
Q

What is the kidney endocrine function with prostaglandin?

A

Paracrine secretion vasodilates the afferent arterioles to increase GFR

308
Q

What can NSAIDS cause in the kidney?

A

NSAIDS can cause acute renal failure by inhibiting the renal production of prostaglandins, which keep the afferent arterioles vasodilated to maintain GFR

309
Q

What is the effect of ANP on the nephron?

A

Causes increased GFR and increased sodium filtration at the proximal tubule with no compensatory sodium reabsorption in the distal nephron
Net effect is sodium loss and volume loss

310
Q

List 6 things that cause a shift of potassium out of the cell causing hyperkalemia

A
  1. Digitalis
  2. Hyperosmolarity
  3. insulin deficiency (ie diabetic ketoacidosis)
  4. lysis of cells
  5. Acidosis (via H/K pump)
  6. Beta adrenergic antagnosits
311
Q

Lost three things that can treat hyperkalemia

A

Albuterol
Insulin (give dextrose first!)
Bicarb

312
Q

List 4 things that shifts potassium into the cells causing hypokalemia

A
  1. Hypo-osmolarity
  2. insulin (increased Na/K ATPase)
  3. Alkalosis
  4. Beta adrenergic agonist (increased Na/K ATPase)
313
Q

Compare what happens with low and high serum sodium levels?

A

Low - nausea and malaise, stupor and coma

High - irritability, stupor, coma

314
Q

Compare what happens with low and high serum Potassium levels?

A

Low - U waves on ECG, flattened T waves, arrhythmias, muscle weakness

High - Wide QRS and peaked T waves on ECG, arrhythmias and muscle weakness

Remember that T waves mirror K+ levels

315
Q

Compare what happens with low and high serum calcium levels?

A

Low - tetany, seizures, positieve trousseau sign, Chvostek sign

High - Stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not nevessarily calciuria

Remember, decreased extracellular calcium leads to INCREASED membrane excitability

316
Q

Compare what happens with low and high serum Magnesium levels?

A

Low - tetany, arrhythmias can lead to torsades de pointes

High - decreased deep tendon reflexes, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

317
Q

Compare what happens with low and high serum phosphate levels?

A

Low - Bone loss and osteomalacia

High - Renal stones, metastatic calcifications, hypocalcemia

318
Q

What should be seen with a compensatory mechanism in a acid-base disturbance?

A

A compensatory mechanism should never bring the pH all the way back into the normal rage.
If it’s normal and PCO2 and bicarb are both wacked then most likely its a mixed situation.

319
Q

What is the Winter’s formula?

A

PCO2 = 1.5 (bicarb) + 8 plus or minus 2

320
Q

When is the Winter’s formula used?

A

Winter’s formular predicts the respiratory compensation for a simple metabolic acidosis

PCO2 = 1.5 (bicarb) + 8 plus or minus 2

If the measured PCO2 differs significantly from the predicted PCO2, then a mixed acid-base disorder is likely present

321
Q

What 6 things cause hypernatremia?

A 
6 Ds:
Diuretics
Dehyrdation
Diabetes insipidus
Docs (iatrogenic)
Diarrhea
Diseases of the kidney
322
Q

What can cause a high anion gap metabolic acidosis?

A 
MUDPILES
Methanol (formic acid)
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tables or INH
Lactic acidosis
Ethylene glycol (oxalic acid)
Salicylates (late)
323
Q

How do you measure anion gap?

A

anion gap = Na - (Cl + biacrb)

normal anion gap = 8-12

324
Q

What can cause a normal anion gap metabolic acidosis?

A 
HARD-ASS
Hyperalimentation
Addison's disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
325
Q

What can cause a respiratory acidosis?

A

Hypoventilation

  • airway obstruction
  • acute lung disease
  • chronic lung disease
  • opioids, sedatives
  • weakening of respiratory muscles
326
Q

What can cause a respiratory alkalosis?

A

Hyperventilation

  • early high altitude exposure
  • Salicylates (early)
  • anxiety, panic attack
  • acute hypoxemia (PE)
327
Q

What can cause a metabolic alkalaosis?

A
  • loop diuretics
  • vomiting
  • antacid use
  • Hyperaldosteronism
328
Q

Describe Type 1 Renal tubular acidosis

A

This is “distal”
Impaired Hydrogen excretion “H” = one letter (type I)
- Defect in collecting tubule’s ability to excrete H
Untreated patients have a urine pH >5.5
associated with hypokalemia.
Increase risk for calcium phosphate stones as a result of increased urine pH and bone resorption

329
Q

What are patients with Type 1 Renal tubular acidosis at increased risk for?

A

Calcium phosphate kidney stones as a result of increased urine pH and bone resorption

330
Q

Describe Type 2 renal tubular acidosis

A

“proximal”
Defect in proximal tubule bicarb reabsorption.
May be seen with fanconi’s syndrome
Uncreated patients typically have a urine pH <5.5 associated with hypokalemia
Increased risk for hypophosphatemic rickets

331
Q

What are patients with type 2 renal tubular acidosis at increased risk for?

A

Increased risk for hypophosphatemic rickets

332
Q

Describe Type 4 renal tubular acidosis

A

“Hyperkalemic”
Hypoaldosteronism or lack of collecting tubule response to aldosterone.
The resulting hyperkalemia impairs ammoniagenesis in the proximal tubule leading to decreased buffering capacity and decreased urine pH
Can’t generate NH4+

333
Q

What is the mnemonic for remembering the defect with Type 4 renal tubular acidosis?

A

Impaired ammonium excertion

“NH4” (4) or low ALDOsterone (4 letters)

334
Q

What is the defect in type 2 renal tubular acidosis similar to?

A

Similar to the effects of Acetazolamide

335
Q

What is seen with bladder cancer and kidney stones?

A

Hematuria with no casts

336
Q

What is seen in acute cystitis?

A

pyuria with no casts

337
Q

What do seeing casts in the urine mean?

A

Presence of casts indicates that hematuria/pyuria is of renal (vs blader) origin

338
Q

With what conditions would you see RBC casts?

A

Glomerulonephritis, ischemia, or malignant hypertension

339
Q

With what conditions would you see WBC casts?

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

340
Q

With what conditions would you see Fatty casts (“oval fat bodies”)?

A

Nephrotic syndrome

341
Q

With what conditions would you see granular (“muddy brown”) casts?

A

Acute tubular necrosis

342
Q

With what conditions would you see waxy casts?

A

Advanced renal disease/chronic renal failure

note that the most common cause of chronic renal failure is poorly controlled diabetes

343
Q

With what conditions would you see Hyaline casts?

A

Nonspecific, can be a normal finding

Hyaline casts are solidified Tamm-Horsfall protein secreted from tubular epithelial cells

344
Q

Which two kidney diseases can be seen as both Nephritic and Nephrotic syndromes?

A

Diffuse proliferative glomerulonephritis

Membranoproliferative glomerulonephritis

345
Q

Why do you see lipiduria/oval fat bodies in nephrotic syndrome?

A

You have massive proteinuria resulting in decreased plasma proteins which leads to edema
Because you depleted the serum albumin and lose the colloid oncotic pressure, the liver tries to compensate by generating lipids in an attempt to maintain osmotic pressure gradient

346
Q

Describe the findings in a patient with Nephrotic syndrome

A

A patient presents with massive proteinuria (>3.5 g/day) and frothy urine. They have hyperlipidemia, fatty casts and edema.
They also have thromboembolism due to a loss of ATIII in the urine
and increased risk of infections due to loss of immunoglobulin in the urine

347
Q

Why are patients with nephrotic syndrome hypercoagulable?

A

They have a lost of AT III in their urine making them have thromboembolisms

348
Q

Why do patients with nephrotic syndrome have an increased risk of infection?

A

Immunoglobulinuria

349
Q

A patient presents with massive proteinuria (>3.5 g/day) and frothy urine. They have hyperlipidemia, fatty casts and edema.

A

Nephrotic syndrome

350
Q

Light microscopy shows segmental sclerosis and hyalinosis - what will you see on EM?

A

This is focal segmental glomerulosclerosis

EM will show effacement of foot processes similar to minimal change disease

351
Q

What is the most common cause of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis

352
Q

What is the most common cause of nephrotic syndrome in latinos and African americans?

A

Focal segmental glomerulosclerosis

353
Q

What 5 things are associated with focal segmental glomerulosclerosis?

A 
HIV infection
Heroin abuse
Massive obesity
interferon treatment
chronic kidney disease due to congenital absence or surgical removal
354
Q

Light microscopy shows diffuse capillary and diffuse glomerular basement thickening, what will you see on EM?

A

This is membranous nephropathy

EM will show spike and dome appearance with subepithelial deposits

355
Q

What is seen on immunofluorescence in Membranous nephropathy?

A

Granular

356
Q

What is the second most common cause of primary nephrotic syndrome in adults?

A

Membranous nephropathy

357
Q

What is the nephropathy presentation of an SLE patient?

A

Membranous nephropathy

358
Q

What is deposited and where in a patient with membranous nephropathy?

A

Subepithelial deposits of IgG, C3, K and lambda light chains

note that the mesangium is normal

359
Q

A patient presents with normal glomeruli on light microscopy, what will be seen on EM?

A

This is minimal change disease (lipoid nephrosis)

EM will show foot process efacement

360
Q

What is lost in a patient with minimal change disease?

A

Selective loss of albumin but not globulins

caused by GBM polyanion loss

361
Q

A patient presents with a recent infection or immunization - what nephropathy are they at risk of getting?

A

Minimal change disease
Most common in children.
responds well to corticosteroids

362
Q

A patient presents with congo red stain showing birefringence under polarized light due to mesangial deposits of what?

A

This is amyloidosis causing a nephrotic syndrome

363
Q

What can cause amyloidosis nephropathy?

A

A chronic condition like multiple myeloma, TB or rheumatoid arthritis

364
Q

Describe the differences between Type I and Type II membranoproliferative glomerulonephritis

A

Type 1 - subendothelial immune complex deposits with granular immunofluorescence. Shows “tram track” appearance due to GBM splitting caused by mesangial ingrowth

Type II - Intramembranous immune complex deposits

365
Q

What is type 1 membranoproliferative glomerulonephritis associated with?

A

HBV and HCV

366
Q

What is type 2 membranoproliferative glomerulonephritis associated with?

A

C3 nephritic factor

367
Q

Proliferation of mesangial and endothelial cells of the glomeruli and expansion of the mesangial matrix along with immune deposits

A

membranoproliferative glomerulonephritis

368
Q

What occurs in diabetic glomerulonephropathy?

A

Nonenzymatic glycosylation of the glomerular basement membrane leading to increased permeability and thickening

369
Q

What occurs in diabetic glomerulonephropathy at the efferent arterioles?

A

Nonenzymatic glycosylation of the efferent arteriole leads to increased GFR and then to mesangial expansion

370
Q

What is seen on light microscopy with a patient with diabetic glomerulonephropathy?

A
  • Mesangial expansion, glomerular basement membrane thickening
  • eosinophilic nodular glomerulosclerosis = Kimmelstiel-Wilson nodules
371
Q

Describe the common presentation seen in nephritic syndrome

A

Inflammatory process
When it involves the glomeruli, it leads to hematuria and RBC casts in the urine. Associated with azotemia, oliguria, hypertension and proteinuria (<3.5 g/day)

372
Q

A patient presents with inflammation and hematuria and RBC casts in the urine. Associated with azotemia, oliguria, hypertension and proteinuria (<3.5 g/day)

A

Nephritic syndrome

373
Q

What type of hypersensitivity is acute postsreptococcal glomerulonephritis?

A

Type III HS

Immune complexes get deposits in the glomeruli

374
Q

A patient presents with glomeruli enlarged and hypercellular, neutrophils within the glomerulus and a “lumpy bumpy” appearance - what would be seen on EM?

A

This is acute poststreptococcal glomerulonephritis

EM would show subepithelial immune complex humps

375
Q

What does the IF show in poststreptoccocal glomerulonephritis?

A

granular appearance due to IgG, IgM and C3 deposition along the GBM and mesangium

376
Q

What is the clinical findings in a patient with poststreptococcal glomerulonephritis? What test should you do?

A

Most frequently seen in children.
Peripheral and periborbital edema, dark urine (Coca-Cola colored) and hypertension.
Resolves spontaneously
An anti-streptolysin O titer would confirm diagnosis

377
Q

A patient gets a group A beta hemolytic strep infection - giving them antibiotics will protect them against what?

A

Rheumatic fever and rheumatic heart disease

but it will NOT protect against poststreptococcal glomerulonephritis

378
Q

Light microscopy shows crescent moon shapes within a glomerulus and the patient has rapidly deteriorating renal function - what is contained within the crescents and what is the diagnosis?

A

Rapidly progressive (crescentic) glomerulonephritis

The crescents consist of fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages

379
Q

List three diseases that can present with Rapidly progressive (crescentic) glomerulonephritis?

A
  • Goodpasture’s syndrome - type II HS with antibodies tot GBM and alveolar basement membrane giving a linear IF
  • Granulomatosis with polyangiitis (Wegener’s) - c-ANCA +
  • Microscopic polyangiitis - p-ANCA +
380
Q

What is the most common cause of death in SLE patients?

A

Diffuse proliferative glomerulonephritis

381
Q

List two things that can cause Diffuse proliferative glomerulonephritis?

A
  1. SLE

2. Membranoproliferative glomerulonephritis

382
Q

Light microscopy shows wire looping of capillaries - what will be seen on EM and IF?

A

This is diffuse proliferative glomerulonephritis
EM will show subendothelial and sometimes intramembranous IgG based immune complexes often with C3 deposition
IF will be granular

383
Q

A patient has Henoch-Schonlein purpura, what nephritic syndrome are they most likely to get?

A

Berger’s disease (IgA nephropathy)

384
Q

What will be seen in LM, EM and IF in a patient with Berger’s disease?

A

LM - Mesangial proliferation
EM - Mesangial immune complex deposits
IF - IgA based immune complex deposits in the mesangium

385
Q

What is the tetrad seen in Berger’s disease?

A

palpable purpura on the butts and legs
arthralgias
abdominal pain
renal disease

386
Q

What causes Berger’s disease?

A

Often presents/flares with a URI or acute gastroenteritis

387
Q

A patient presents with glomerulonephritis, deafness and eye problems - what is the diagnosis?

A

Alports syndrome (AKA hereditary nephritis)

388
Q

What is the defect in Alports syndrome - and what does it cause in the kidney?

A

Mutation in type IV collagen leading to split basement membrane
X-linked

389
Q

What is the outcome of a patient with rapidly progressive crescentic glomerulonephritis?

A

poor prognosis, rapidly deteriorating renal function (days to weeks)

390
Q

What is the most common type of kidney stone?

A

Calcium oxalate

391
Q

What causes precipitation of calcium oxalate stone?

A

decreased pH

392
Q

What causes precipitation of calcium phosphate stone?

A

increased pH

393
Q

Which stone is radiolucent on Xray?

A

Uric acid stone

394
Q

What can cause calcium oxalate stones?

A

oxalate crystals can result from ethylene glycol (antifreeze) or vitamin C abuse

395
Q

What is the treatment for calcium kidney stones?

A

thiazides and citrate for recurrent stones

396
Q

What is the most common kidney stone presentation?

A

calcium oxalate stone in a patient with hypercalciuria and normocalcemia

397
Q

what can generally cause calcium stones if a patient hasn’t ingested anything bad..?

A

conditions that cause hypercalcemia (cancers, increased PTH), things that can increase calciuria

398
Q

What pH do ammonium magnesium phosphate stones precipitate at?

A

increased pH

399
Q

What causes ammonium magnesium phosphate stones?

A

caused by infection with urease-positive bugs like proteus mirabilis, staphylococcus and klebsiella
They hydrolyze urea to ammonia leading to urine alkalinization

400
Q

What is a common cause of staghorn calculi?

A

ammonium magnesium phosphate (struvite) stones

401
Q

Uric stones are radiolucent on Xray - is there another way to see them?

A

they are visible on CT and ultrasound

402
Q

When do you see uric acid stones?

A
  • stone association with hyperuricemia ( gout)

- often seen in diseases with increased cell turnover like leukemia

403
Q

At what urine pH do you see uric acid stones?

A

decreased pH

404
Q

What is the treatment of uric acid stones?

A

alkalinization of the urine

405
Q

At what pH do you see cystine stones?

A

Precipitates at decreased pH

causes hexagonal crystals

406
Q

What causes cystine stones?

A

most often secondary to cystinuria.

407
Q

How do you treat cystine stones?

A

Alkalinization of the urine

408
Q

A 36 yo F has kidney stones and she gets pain in her right flank to her groin - what is a muscle that’s being affected as part of a viscerosomatic response?

A

psoas MAJOR

409
Q

Describe hydronephrosis

A

Backup of urine into the kidney.
Can be cuased by urinary tract obstruction or vescoureteral reflux.
causes dilation of renal pelvis and calyces proximal to obstruction.
May result in parenchymal thinning in chronic severe cases

410
Q

what cells to renal cell carcinoma originate from?

A

Originates from proximal tubule cells

this is why they are polygonal clear cells filled with accumulated lipids and carbohydrates

411
Q

how does renal cell carcinoma manifest clinically?

A

Hematuria, palpable mass, secondary polycythemia (XS EPO), flank pain fever and weight loss

412
Q

Who gets renal cell carcinoma?

A

Most common in men 50-70 yo with increased incidence with smoking and obesity

413
Q

Where does renal cell carcinoma spread to?

A

It invades the renal vein then the IVC and spreads hematogenously
Metastasizes to lung and bone

414
Q

How do you treat renal cell carcinoma/

A

resection is it’s localized

it’s resistant to conventional chemotherapy and radiation therapy

415
Q

what gene deletion is renal cell carcinoma associated with?

A

gene deletion on chromosome 3 (deletion may be sporadic or inherited as von hippel-lindau syndrome)

416
Q

What can cause a nephroblastoma?

A

This is a Wilms’ tumor
deletion of tumor suppressor gene WT1 on chromosome 11
May be part of Beckwith-Wiedemann syndrome or WAGR complex

417
Q

What is the most common renal malignancy of early childhood (2-4 yo)?

A

Wilm’s tumor (nephroblastoma)

418
Q

How does a nephroblastoma present?

A

huge palpable flank mass and/or hematuria in a 2-4 yo

note that it will contain embryonic glomerular structures

419
Q

What is the most common tumor of the urinary tract system and where can it occur?

A

Transitional cell carcinoma

can occur in renal calyces, renal pelvis, ureters, and bladder

420
Q

What suggest bladder cancer?

A

Painless hematuria (no casts!)

421
Q

What can cause transitional cell carcinoma?

A 
Associated with problems in your P SAC
Phenacetin
Smoking
Aniline dyes
Cyclophosphamide
422
Q

A patient presents with fever, costovertebral angle tenderness, nausea and vomiting with white cell casts in the urine - what’s happening?

A

Acute pyelonephritis

affects the cortex with relative sparing of the glomeruli/vessels

423
Q

What causes coarse, asymmetric corticomedulalry scarring with blunted calyces and tubules that contain eosinophilic casts?

A

Chronic pyelonephritis

thyroidization of the kidney!

424
Q

What causes chronic pyelonephritis?

A

recurrent episodes of acute pyelonephritis

typically requires predisposition to infection like vescoureteral reflux or chronically obstruction kidney stones

425
Q

What causes drug induced interstitial nephritis?

A

AKA tubulointerstitial nephritis

drugs that act as haptens, inducing hypersensitivity

nephritis typically occurs 1-2 weeks after certain drugs are given but can occur months after starting NSAIDS

426
Q

What drugs can cause drug induced interstitial nephritis?

A

diuretics, penicillin derivatives, sulfonamides, rifampin and NSAIDs

427
Q

what is the clinical findings in drug induced interstitial nephritis?

A

associated with fever, rash, hematuria, and costovertebral angle tenderness or it can be asymptomatic.
often see pyuria (classically eosinophils) and azotemia

428
Q

What is diffuse cortical necrosis?

A

Acute generalized cortical infarction of BOTH kidneys likely due to a combination of vasospasm and DIC

429
Q

What is diffuse cortical necrosis associated with?

A

Associated with obstetric catastrophes and septic shock

430
Q

What is the key finding in a patient with acute tubular necrosis?

A

granular muddy brown casts

431
Q

What is the most common cause of intrinsic renal failure?

A

Acute tubular necrosis

432
Q

What is the result in someone with acute tubular necrosis?

A

It’s self reversible in some cases but can be fatal if left untreated
death most often occurs during the initial oliguric phase

433
Q

List the 3 stages of acute tubular necrosis

A
  1. inciting event
  2. maintenance phase - oliguric; lasts 1-3 weeks; risk of hyperkalemia
  3. Recovery phase - polyuric; BUN and serum creatinine fall; risk of hypokalemia
434
Q

What is acute tubular necrosis associated with?

A

renal ischemia like shock and sepsis, crush injury (myoglobinuria), drugs and toxins

435
Q

Describe renal papillary necrosis

A

Sloughing of renal papillae leading o gross hematuria and proteinuria. May be triggered by a recent infection or immune stimulus

436
Q

What is renal papillary necrosis associated with?

A

Diabetes mellitus
Acute pyelonephritis
Chronic phenacetin use (acetaminophen is phenacetin derivative)
Sickle cell anemia and trait

437
Q

how is acute renal failure defined?

A

abrupt decline in renal function with increased creatinine and increased BUN over a period of several days

438
Q

Describe prerenal azotemia?

A

As a result of decreased RBF leading to decreased GFR

sodium and water and urea are retained by the kidney in an attempt to conserve volume so BUN/Cr ratio increase

439
Q

List 4 things that can cause pre-renal azotemia

A

Hypovolemia
Shock
hypotension
renal vasoconstriction with NSAIDs

440
Q

Describe intrinsic renal failure

A

generally due to acute tubular necrosis or ischemia/toxins; less commonly due to acute glomerulonephritis.
Patchy necrosis leads to debris obstructing the tubule and fluid backflow across the necrotic tubule
- decreased GFR
- urine has epithelial/granular casts
-Buns reabsorption is impaired leading to decreased BUN/Cr ratio

441
Q

List 5 things that can cause intrinsic renal failure

A 
Acute interstitial necrosis
glomerulonephritis
acute tubular necrosis
DIC
acute pyeonephritis
442
Q

Describe postrenal azotemia

A

Due to outflow obstruction. develops only with BILATERAL obstruction

443
Q

List 4 things that can cause postrenal azotemia

A

Stones
BPH
neoplasia
congenital anomalies

444
Q

Describe the urine osmolarity, urine sodium, FENA, and serum BUN/Cr seen in prerenal azotemia?

A

Urine osmolarity: >500
Urine sodium: < 20
FENA: 20

445
Q

Describe the urine osmolarity, urine sodium, FENA, and serum BUN/Cr seen in intrinsic azotemia?

A

Urine osmolarity: 40
FENA: >2%
Serum BUN/Cr: < 15

446
Q

Describe the urine osmolarity, urine sodium, FENA, and serum BUN/Cr seen in postrenal azotemia?

A

Urine osmolarity: 40
FENA: >2%
Serum BUN/Cr: >15

447
Q

What are some commonly seen things in renal failure?

A 
Hyperkalemia, hypocalcemia 
Metabolic acidosis
Uremia (increased BUN and creatinine)
Anemia
Renal osteodystrophy
Dyslipidemia
Hyperphosphatemia
448
Q

What is renal osteodystrophy?

A

Failure of vitamin D hydroxylation, hypocalcemia, and hyperphosphatemia leading to secondary hyperparathyroidism

449
Q

What is seen in renal osteodystrophy?

A

Hyperphosphatemia can independently decreased serum calcium but causing tissue calcifications, whereas decreased vitamin D leads to decreased intestinal calcium absorption

causes subperiosteal thinning of bones

450
Q

A patient presents with flank pain, hematuria, hypertension, urinary infection and progressive renal failure - what disease do they have?

A

ADPKD

451
Q

What is ADPKD?

A

Multiple, large bilateral cysts that ultimately destroy the kidney parenchyma

452
Q

What is the mutation in ADPKD?

A

AD mutation in PKD1 or PKD2

453
Q

What 3 findings are associated with ADPKD?

A

Berry aneurysms
mitral valve prolapse
benign hepatic cysts

454
Q

What causes death in patients with ADPKD?

A

death from complications of chronic kidney disease or hypertension (caused by increased renin)

455
Q

What is ARPKD?

A

Infantile presentation in parenchyma

significant renal failure in utero can lead to Potter’s syndrome

456
Q

What is ARPKD associated with?

A

congenital hepatic fibrosis

457
Q

What are the concerns with ARPKD beyond the neonatal period?

A

hypertension, portal hypertension, progressive renal insufficiency

458
Q

What is medullary cystic disease?

A

inherited disease causing tubulointerstital fibrosis and progressive renal insufficiency with inability to concentrate the urine
has poor prognosis

459
Q

What is seen on PE with medullary cystic disease?

A

medullary cysts usually no visualized but shrunken kidneys can be seen on ultrasound

460
Q

What part of the kidney does mannitol and acetazolamide work?

A

Proximal convoluted tubule

461
Q

What is the MOA of mannitol?

A

Causes increased serum osmolarity so it acts as an osmotic diuretic, causes increased tubular fluid osmolarity producing increased urine flow
also decreases intracranial and intraocular pressure

462
Q

What are the clinical uses of mannitol?

A

Drug overdose, elevated intracranial/intraocular pressure

463
Q

What is the MOA of acetazolamide?

A

Carbonic anhydrase inhibitor

464
Q

What does Acetazolamide cause?

A

self limited sodium bicarcb diuresis and reduction in total body bicarb stores

465
Q

What are the clinical uses of Acetazolamide?

A
  • Chronic glaucoma (bicarb helps to pull fluid into the eye to make aqueous humor)
  • Urinary alkalinization
  • altitude sickness
  • metabolic alkalosis
  • pseudotumor cerebri
466
Q

What are the side effects seen with Mannitol?

A

Pulmonary edema, dehydration

note mannitol is contraindicated in anuria (renal failure) and CHF

467
Q

What are the side effects seen with Acetazolamide?

A

Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy

“ACID”azolamide causes ACIDoses

468
Q

Where do loop diuretics like Furosemide and ethacrynic acid have their effects?

A

thick ascending limb of loop of henle

469
Q

What is the MOA of Furosemide?

A
  • Inhibits cotransport system (Na, K, 2CL) of thick ascending limb of loop of Henle.
  • Abolishes hypertonicity of the medulla preventing concentration of urine
  • Stimulates PGE release (vasodilatory effect on afferent arteriole), inhibited by NSAIDS
  • Increases calcium excretion ( LOOPS LOSE CALCIUM!)
470
Q

What is the clinical use of Furosemide?

A

Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia

471
Q

What is the problem with Furosemide?

A

It’s a sulfonamide!

472
Q

What is the toxicity seen with furosemide?

A 
LOOPS? OH DANG!
Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout
473
Q

What is Ethacrynic acid and it’s MOA?

A

It’s a loop diuretic but it’s not a sulfa drug, instead it’s a penoxyacetic acid derivative
it has essentially the same action as furosemide

474
Q

What’s the clinical use of Ethacrynic acid?

A

diuresis in patients allergic to sulfa drugs

475
Q

What is the toxicity seen in Ethycrynic acid?

A

Similar to furosemide, can cause hyperuricemia

never use to treat gout!

476
Q

Where in the nephron does Hydrochlorothiazide work?

A

Distal convoluted tubule

477
Q

What is the MOA of thiazides?

A

Inhibits NaCl reabsorption in the early distal tubule, reducing diluting capacity of the nephron

478
Q

What’s the difference between thiazides in loop diuretics when it comes to calcium?

A

Loops LOSE calcium and thiazides retain calcium

479
Q

What are the clinical uses of thiazides?

A

HYPERTENSION!

CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus

480
Q

What are the toxicities seen with thiazide diuretics?

A

Hypokalemic metabolic alkalosis
hyponatremia

HyperGLUC 
hyperGlycemia
hyperLipidemia
HyperUricemia 
hyperCalcemia

note that thiazide diuretics are sulfa drugs!

481
Q

Name 4 potassium sparing diuretics

A

“Potassium, please have a SEAT”

Spironolactone
Eplerenone
Amiloride
Triamterene

482
Q

What is the MOA of spironolactone and eplerenone?

A

competitive aldosterone receptor antagonists in the cortical collecting tubule

483
Q

What is the MOA of triamterene and amiloride?

A

Act in the cortical collecting tubule to block sodium channels ( block eNaC)

484
Q

What is the clinical use of potassium sparing diuretics?

A

Hyperaldosteronism, Potassium depletion, CHF

you can give it with a loop diuretic to retain potassium

485
Q

What is the toxicity seen with potassium sparing diuretics?

A

Hyperkalemia that can lea to arrhythmias

endocrine effects with spironolactone (gynecomastia, antiandrogen effects)

486
Q

Why don’t you see antiandrogen effects with eplerenone like you do with spironolactone?

A

Eplerenone is more specific for the mineralocorticoid receptor

487
Q

Diuretic effects on urine NaCl?

A

Increased with all diuretics except acetazolamide

Serum sodium may decrease as well

488
Q

Diuretic effects on urine K+?

A

Increased in all except potassium sparing diuretics

serum potassium may decrease as well

489
Q

Why do you see metabolic acidosis with carbonic anhydrase inhibitors and with potassium sparing diuretics?

A

Carbonic anhydrase inhibitors - decrease bicarb reabsorption

Potassium sparing diuretics - aldosterone blockade prevents K secretion and H+ secretion. Additionally, hyperkalemia lead to K entering all cells (via H/K exchanger) in exchange for H exiting the cells

490
Q

Why do you see metabolic alkalosis in thiazides and loop diuretics?

A

Several mechanisms:

  • Volume contraction leads to increased ATII which leads to increased Na/H exchange in proximal tubule leading to increased bicarb reabsorption (contraction alkalosis)
  • K loss leads to K exiting cells in exchange for H entering cells
  • In low K state, H (rather than K) is exchanged for Na in cortical collecting tubule leading to alkalosis and paradoxical aciduria
491
Q

why do you lose calcium with loop diuretics?

A

decreased paracellular calcium reabsorption

492
Q

Why do thiazides retain calcium?

A

enhanced paracellular calcium reabsorption in proximal tubule and loop of henle

493
Q

Name 3 ACE inhibitors

A

Captopril, Enalapril, lisinopril

494
Q

in what patients should you avoid using ACE-I?

A

Patients with bilateral renal artery stenosis because ACE inhibitors will further decreased GFR which can lead to renal failuer

495
Q

what is the MOA of ACE inhibitors?

A

Inhibit ACE leading to decreased ATII leading to decreased GFR by preventing constriction of efferent arterioles.
Levels of renin increase as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator

496
Q

list 5 uses of ACE-I?

A 
Hypertension
CHF
proteinuria
diabetic renal disease
Prevents unfavorable heart remodeling as a result of chronic hypertension
497
Q

why are ACE-I beneficial in patients with diabetic renal disease?

A

decreases progression of proteinuria and progression of diabetic nephropathy

498
Q

List the toxicities of ACE-I

A 
Captopril's CATCHH
Cough
Angioedema
Teratogen (fetal renal abnormalities)
Creatinine increase (Decreased GFR)
Hyperkalemia (really only a big deal if you also have you patient on regular doses of aspirin or a potassium sparing diuretic)
Hypotension
499
Q

What is Aliskiren?

A

Renin inhibitor. ONLY indicated for HTN
Can cause hyperkalemia and renal insufficiency
contraindicated in pregnancy

First Aid Chs Part 2 (6 decks)

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