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PATHOMA/FA SYSTEMS > RENAL > Flashcards

RENAL Flashcards

1
Q

What are 3 reasons the parathyroid would secrete PTH?

A

low calcium, high phosphate, or low active vitamin D

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2
Q

How is medullary cystic kidney disease inherited? Discuss the appearance of the kidneys

A

AD; there are cysts in the COLLECTING DUCTS. The parenchyma is fibrosed, the kidneys are shrunken. There is progressive renal disease

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2
Q

What may interstitial nephritis progress to?

A

papillary necrosis (SODA)

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3
Q

What functions as the kidney for the first trimester?

A

mesonephros (eventually becomes part of male reproductive system)

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3
Q

Major cause of death in Potter’s

A

pulmonary hypoplasia

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3
Q

How do you treat uric acid stones and cystine stones?

A

alkalinize the urine (NaHCO3)

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3
Q

What syndrome is associated with renal cell CA?

A

Von Hippel Lindau

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3
Q

What are the 4 aspects of Beckwith-Weidmann syndrome (gene and chromosome?)

A

Wilm’s tumor, Aniridia, Genitourinary malformation, MR; WT1 gene on chromosome 11

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3
Q

What are the 3 stages of acute tubular necrosis?

A

Inciting phase; Maintenance phase (oliguria for 1-3 weeks with hyperkalemia risk) and then Recovery phase (polyuria with decrease in BUN creatinine and the risk of hypokalemia)

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3
Q

Explain how the hyperphosphatemia of renal osteodystrophy leads to further decrease of Ca

A

It binds it up and causes metastatic tissue calcifications

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3
Q

What effect does constriction of the ureter have on 1) RPF 2) GFR 3) FF

A

1) no change 2) decrease 3) decrease

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3
Q

How do you measure the anion gap? What is normal?

A

Na - (Cl +HCO3)

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3
Q

Why does BUN increase in pre-renal azotemia?

A

The low flow leads to a decrease in GFR with increased water reabsorption, thus, increased BUN since urea follows water

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3
Q

What is the most commonly involved organ in systemic amyloidosis

A

kidney

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4
Q

What do fatty casts in urine indicate?

A

Nephrotic syndrome (oval fat bodies)

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4
Q

Ballooning degeration in kidney

A

Toxic cause (acute interstitial nephritis or acute tubular necrosis from toxin)

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5
Q

What is the deal with medullary cystic kidney?

A

inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine

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5
Q

What is the response of most nephrotic syndromes to steroids?

A

Poor with progression to CKD; except minimal change dz

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6
Q

Which PKD is associated with liver cysts? Congenital hepatic fibrosis?

A

ADPKD; ARPKD (can lead to portal HTN)

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6
Q

What is the hallmark of nephritic syndrome?

A

glomerular bleeding

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7
Q

Which nephrotic syndrome responds well to steroids?

A

Minimal change disease

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7
Q

8 causes of wide anion gap metabolic acidosis (MUD PILES)

A

Methanol, Uremia, DKA, Propylene glycol, Iron tablets and Isoniazid, Lactic acidosis, Ethylene glycol, and Salycylates late

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8
Q

What is absorbed via paracellular route in the TALH? Why?

A

Mg and Ca because the NKCC channel creates a positive lumen due to K backleak, this shoves Ca and Mg through

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8
Q

What are 2 causes for aldosterone synthesis?

A

AT II in result to blood loss or hyperkalemia

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8
Q

What is the hallmark of acute renal failure?

A

azotemia (increased BUN AND creatinine) also oliguria

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9
Q

Why do you give DM the “benefit” of the ACE I?

A

DM nephropathy involves hyalinization preferentially of the efferent arteriole (prob bc the sugar has more time to chill there). ACE-I prevent constriction of the efferent arteriole; this decreases hyperfiltration injury

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10
Q

Which casts are seen in bladder cancer and kidney stones?

A

no casts, just hematuria

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10
Q

Which nephritic syndrome follows gastroenteritis?

A

Berger’s IgA nephropathy (mesangial deposits)

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10
Q

Give a basic explanation for the dry cough of ACE I

A

ACE degrades bradykinin, lose of ACE involves buildup of bradykinin

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12
Q

3 syndromes with Wilms tumor

A

Beckwith-Weidmann syndrome; Denys-Drash syndrome; WAGR syndrome

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13
Q

Thyroidization of the kidney

A

Eosinophilic casts in chronic pyelonephritis give it the look of thyroid follicles

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13
Q

What is the value for Tm of glucose?

A

350

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14
Q

Which is reabsorbed, BUN or creatinine?

A

BUN for countercurrent exchange. So if both BUN and creatinine go up that is renal failure

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14
Q

What is type 4 renal tubular acidosis?

A

Hypoaldosteronism (Addison’s) or lack of response to aldosterone at CD? The hyperkalemia impairs ammoniagenesis in the PCT leading to decreased buffering capacity and a low urine pH? However, this still causes a metabolic acidosis

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15
Q

Which nephritic syndrome splits the basement membrane? (2)

A

Acquired = MPGN I due to mesangial proliferation that splits GBM, this can present nephritic or nephrotic; INHERITED = Alport Syndrome, an XR collagen 4 defect that leads to splitting

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15
Q

Name 3 urease positive bugs that can cause struvite stones

A

PROTEUS!!!! And Staphylococcus and Klebsiella

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15
Q

Why is there hyperkalemia and metabolic acidosis in CKD?

A

Because there is a decreased ability to secrete organic acids and because you don’t secrete as much K, the cells exchange K for H

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15
Q

What is cystitis glandularis? Risk?

A

Columnar (glandular) metaplasia of transitional urothelium; increase risk of adenocarcinoma

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16
Q

Which embryological structure is responsible for most of the kidney as distal as the DCT?

A

intermediate mesoderm? i.e. metanephric mesenchyme? The ureteric bud makes up the calyces

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17
Q

What causes hexagonal stones?

A

Cystine (secondary to cystinuria, a defective PCT transporter for cysteine, ornithine, lysine, and arginine

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18
Q

Why does Crohn’s Dz increase the risk of kidney stones?

A

mucosal damage increases oxalate absorption from the gut leading to calcium oxalate stones

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19
Q

In essence how should you interpret a TF/P curve?

A

This is tubular fluid/plasma; Basically, if the concentration is higher in TF than P, water was reabsorbed faster than the solute. In other words, it is excreted.

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20
Q

What is multicystic dysplastic kidney?

A

Arises from weird interaction between the ureteric bud and the metanephric mesenchyme. It causes a nonfunctional kidney. If unilateral it will result in contralateral hypertrophy

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20
Q

What is the difference between a primary glomerular disease and a secondary glomerular disease?

A

A primary glomerular disease only affects the kidney (e.g. minimal change disease)? A secondary glomerular disease affects other organs as well (SLE, diabetic nephropathy)

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21
Q

What do muddy brown casts indicate?

A

Acute tubular necrosis (granular casts)

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22
Q

What is type 2 renal tubular acidosis?

A

“proximal”? this is a defect in HCO3 reabsorption and may be seen in Fanconi’s. This is associated with hypokalemia and may increase the risk of hypophosphatemic rickett’s

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23
Q

Which type of urothelial CA is associated with p53 mutations?

A

Flat; papillary is not? So flat urothelial CA is much more serious and harder to Dx

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24
Q

What makes up the crescents in rapidly progressive glomerulonephritis?

A

Fibrin and macrophages

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25
Q

What do you see in the following for membranous nephropathy: LM; EM; and IF?

A

LM = diffuse capillary and GBM thickening; EM = subepithelial deposits with spike and dome; IF = granular

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25
Q

What are the kidney delayed compensations in respiratory alkaloses and acidoses?

A

Alkalosis = decreased reabsorption of HCO3 (reason for giving acetazolamide in altitude sickness); Acidosis = increased HCO3 reabsorption

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26
Q

T/F: polycystic kidney disease can cause Potter’s

A

True but only ARPKD

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26
Q

What EKG findings are present in hypokalemia? Hyperkalemia?

A

Hypo = flat T waves and U waves, arrhythmias; Hyper = peaked T-waves, wide QRS, arrhythmias

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28
Q

What are the 2 most common causes of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis and membranous nephropathy

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30
Q

What causes the hypertension in nephritic syndrome?

A

Salt retention since there is oliguria? Same reason there is azotemia!

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31
Q

What is diffuse cortical necrosis of the kidneys? Cause?

A

acute generalized necrosis of the cortices of both kidneys? usually from vasospasm and DIC (obstetric complications, abruptio placentae)

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32
Q

What effect does PTH have on the PCT? DCT?

A

At PCT, PTH inhibits phosphate reabsorption; at DCT, PTH increases calcium reabsorption via a Ca/Na exchanger

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33
Q

Which MPGN is associated with C3 nephritic factor?

A

Type II dense deposits

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34
Q

What is type 1 renal tubular acidosis

A

“distal”? This is a defect in the ability to secrete H? This increases the risk for Calcium phosphate stones as a result of both increased urine pH and bone resorption (acidic environment)

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35
Q

Subendothelial deposits with nephrotic syndrome are associated with what 2 infections?

A

HBV and HCV (this is MPGN I)

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36
Q

What is the main concern during the recovery phase of acute tubular necrosis?

A

hypokalemia; this is when they start peeing again

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37
Q

Where are juxtaglomerular cells located? Where are macula densa cells located?

A

JG = afferent arteriole; MD = DCT

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38
Q

What if you have cystitis that smells like ammonia?

A

Proteus since converts NH3 to CO2 and ammonia

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39
Q

What is the most important (trump card) reason for ADH secretion?

A

Low blood volume, but more commonly it is to regulate osmolarity

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40
Q

What is the prognosis for crescentic glomerulonephritis?

A

Poor if Rapidly Progressive Glomerulonephritis, can lead to deteriorating renal fxn in days to weeks

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42
Q

genetics of ADPKD

A

Autosomal Dominant, PKD1 gene chromosome 16

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43
Q

What is the filtration fraction?

A

GFR/RPF (the only way to change it is to change one but not the other)

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44
Q

What are 3 causes of rapidly progressive (crescentic) glomerulonephritis?

A

Goodpasture’s disease (type II hypersens)? Pauci-immune glomerulopathies = Wegner’s (c-ANCA) and Microscopic Polyangiitis (p-ANCA)

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46
Q

What is the diagnosis of renal Bx with LM = diffuse capillary and GBM thickening; EM = spike and dome appearance with subepithelial deposits; and IF = granular?

A

Membranous nephropathy (nephrotic)? Presentation of SLE and some solid tumors

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48
Q

What is seen on LM, EM and IF for diffuse proliferative glomerulonephritis?

A

LM = wire looping of capillaries; EM = subendothelial deposits, IF = granular

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48
Q

What other major organ is cystic in ADPKD?

A

liver

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49
Q

What are 3 ways NSAIDs can cause acute renal failure?

A

by inhibiting prostacyclin synthesis in the afferent arteriole leading to decrease in GFR; by causing interstitial nephritis which is a hypersensitivity; also renal papillary necrosis (SODA)

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51
Q

What 2 diseases present as Diffuse Proliferative Glomerulonephritis?

A

SLE (main cause of death in this Dz) and MPGN when presenting as nephritic syndrome

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52
Q

Why are nephrotic syndromes associated with thromboemboli?

A

There is a loss of antithrombin III (heparin may not be effective since it is losing its substrate!!!)

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53
Q

How does PTH cause calcium reabsorption and phosphate excretion?

A

Decrease phosphate reabsorption in PCT; increases Ca reabsorption in DCT

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54
Q

Why are there eosinophils in the urine of interstitial nephritis?

A

It is a hypersensitivity rxn to drugs that act as haptens, so it is a type I hypersensitivity which involves eosinophil chemotactic factor and IL-5

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55
Q

What is uremic frost?

A

deposition of urea crystals in the skin

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56
Q

What would the histology of Goodpasture’s, Wegener’s and Microscopic polyangiitis be on renal Bx?

A

Rapidly progressive (Crescentic) glomerulonephritis; fibrin and plasma proteins make up the crescents, pretty serious!

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57
Q

What does aldosterone do exactly?

A

Aldosterone puts a sodium channel on the luminal side of intercalated cells in the collecting tubules which eventually causes the loss of K. Therfore, K sparing diuretics can either inhibit spironolactone or they may inhibit the Na channel

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58
Q

Which syndrome does membranoproliferative glomerulonephritis present with? Differentiate the appearance of type I and type II

A

Either or both nephritic and nephrotic; Type I = tram-tracking from GBM splitting due to mesangial growth with subendothelial deposits; Type II = intramembranous deposits with “dense deposits” in lamina densa

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60
Q

Pts with Von Hippel Lindau may be polycythemic from EPO production from which 2 tumors?

A

Cerebelllar hemangioblastomas or Renal cell carcinoma

61
Q

Why does the early DCT make the urine hypotonic? Diuretic acting here?

A

Because Na/Cl are actively reabsorbed here; Thiazides

62
Q

What is the concern in ARPKD before birth? After birth?

A

May lead to Potter’s sequence; can cause portal HTN because of congenital hepatic fibrosis, regular HTN from high renin, and progressive renal insufficiency

63
Q

What do WBC casts indicate?

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

65
Q

Why is there glucosuria and aminoaciduria in pregnancy?

A

There is a decrease in the reabsorption of these in pregnancy

65
Q

Where are the kidneys usually connected in horseshoe kidney?

A

lower pole; stuck on IMA

66
Q

What are some classic drugs that cause interstitial nephritis? How long after the drug is administered does it happen?

A

1-2 weeks; diuretics, penicillin derivatives, sulfonamides, and rifampin

67
Q

Which nephropathy is associated with solid tumors? Multiple myeloma?

A

Membranous nephropathy is associated with solid tumors; Amyloidosis is associated with multiple myeloma (and Bence Jones proteins)

67
Q

What is the major concern during the maintenance phase of acute tubular necrosis?

A

hyperkalemia, this is when there is oliguria for 1-3 weeks

67
Q

Explain why amiloride and triamterene are K sparing diuretics that inhibit a sodium channel

A

Because reabsorption of sodium ultimately leads to loss of K and H. Therefore, blocking this channel spares K

69
Q

What conditions predispose to chronic pyelonephritis? Histological finding?

A

Blockages (BPH) and vesicoureteral reflux; thyroidization of kidney, eosinophilic casts in tubules

70
Q

What do RBC casts indicate (3)?

A

Glomerulonephritis, ischemia, and malignant HTN

70
Q

What would you use inulin to measure (water compartment)?

A

extracellular volume, also can measure GFR

71
Q

Which renal disease leads to a cystic kidney due to aberrant interaction between the metanephric mesenchyme and the ureteric bud?

A

Multicystic dysplastic kidney

72
Q

Gross hematuria and proteinuria associated with acute pyelonephritis

A

renal papillary necrosis

74
Q

Which kidney is taken if one wishes to donate?

A

Left kidney, longer renal vein

75
Q

What are the early and late signs of salycylate poisoning

A

Early respiratory alkalosis with a late metabolic acidosis

77
Q

Why does membranous nephropathy cause a spike and dome appearance?

A

There are subepithelial deposits but the podocytes try to lay down more BM leading to a dome on top of them

78
Q

What effect does decreased protein concentration have on 1) RPF 2) GFR 3) FF

A

1) no change 2) increased 3) increased

79
Q

What kind of bladder cancer may arise from chronic cystitis?

A

SCC (not transitional cell)

80
Q

Explain why having a single kidney increases the risk of CKD

A

Because it does the work of two kidneys, this leads to hyperfiltration injury

81
Q

Name 2 cancers that secrete PTHrP

A

SCC of lung; Renal Cell Carcinoma

82
Q

What is the most basic difference between acute and chronic pyelonephritis with respect to the infiltrate?

A

Acute = neutrophils and Chronic = lymphocytes

84
Q

What area is affected in acute pyelonephritis?

A

CORTEX with relative sparing of vessels and tubules

85
Q

What 2 types of stones precipitate in alkaline urine? 3 types in acid?

A

Alkaline = Calcium phosphate and Struvite; Acidic = Calcium oxalate, cystine, and urate

86
Q

Which glomerulopathy has LM = normal glomeruli and EM = podocyte effacement?

A

Minimal change disease (globulins are not lost)

88
Q

What effect does efferent arteriole constriction have on 1) RPF 2) GFR 3) FF

A

1) decrease 2) increase 3) decrease

89
Q

Type of cancer caused by Schistosoma hematobium (specific)

A

SCC of bladder

90
Q

What is contained in the crescents of RPGN?

A

fibrin and plasma proteins

91
Q

Name 5 strictly nephrotic syndromes

A

Focal Segmental glomerulosclerosis, Membranous nephropathy, Minimal change Dz, Amyloidosis, and Diabetic glomerulonephropathy

91
Q

If ischemia is the cause of acute tubular necrosis, what was the likely antecedent cause of azotemia?

A

prerenal azotemia; because it is an ischemic etiology

92
Q

Why are there fatty casts in the urine of nephrotic syndrome?

A

Since so much protein is lost due to the loss of the negative charge barrier, the liver tries to produce more fat to “beef up the blood” these can form fatty casts in renal tubules

93
Q

Risk from bladder exstrophy?

A

adenocarcinoma of bladder

94
Q

Explain how both ANP and ATII maintain GFR but ANP causes natriuresis

A

ANP dilates afferent arteriole leading to increase GFR; AT II constricts efferent arteriole leading to increased GFR; However, only AT II increases the filtration fraction (GFR/RBF), this means only ATII has a compensatory Na reabsorption; therefore, only ANP causes diuresis

96
Q

The first branches off of the renal artery are called ______

A

segmental arteries

97
Q

What would you use radiolabeled albumin to measure?

A

plasma volume

98
Q

What makes up Wilm’s tumor?

A

embryonic glomerular structures

99
Q

How is dysplastic kidney inherited? What kind of tissue is present? How do you differentiated it from PKD?

A

It isn’t it is a MALFORMATION that leads to cysts and CARTILAGE? It is usually lateral, ARPKD is bilateral and ADPKD presents later in life

101
Q

What is the ultimate casue of renal osteodystrophy?

A

Failure to hydroxylate the 1 position on vitamin D

102
Q

Why does acute tubular necrosis and glomerulonephritis cause acute kidney injury (i.e. acute renal failure)

A

Because the stuff that sloughs off gets stuck in the tubules

103
Q

What effect does AT II have on the anterior pituitary?

A

Induces release of ADH

104
Q

What is the purpose of PCT cells generating and secreting ammonia?

A

acts as a buffer for H

106
Q

What is the most common kidney stone presentation?

A

Calcium oxalate in a normocalcemic patient with hypercalciuria (excess PTH)

106
Q

What part of bone is affected in renal osteodystrophy

A

subperiosteal thinning

107
Q

What kind of calcium stones precipitate in alkaline pH? Acidic pH?

A

Alkaline = Calcium phosphate; Acidic = Calcium oxalate (more common)

108
Q

What effect does angiotensin II have on the PCT?

A

stimulates Na/H exchange leading to a contraction alkalosis

109
Q

In the context of nephropathies, what does focal mean? Diffuse? Proliferative? Membranous?

A

Focal = less than 50% glomeruli involved; Diffuse = more than 50% involved, Proliferative = hypercellularity, Membranous = thickening of basment membrane

110
Q

What kidney issue can myoglobinuria cause?

A

Acute Tubular Necrosis

111
Q

What is lost in minimal change disease? What is the finding on LM and EM?

A

Albumin ONLY? LM = normal glomeruli; EM = podocyte effacement

113
Q

What is the gold standard for dx of cystitis?

A

Culture with greater than 100,000 colony forming units

114
Q

What is the most common cause of intrinsic renal failure (i.e. azotemia of the parenchyma)?

A

Acute Tubular Necrosis

116
Q

Why is PAH used to estimate effective renal plasma flow?

A

It is both filtered and secreted

117
Q

Which disease causes cysts in cortex and medulla vs. cysts in collecting ducts?

A

cortex and medulla = PKD (AR and AD); collecting ducts = medullary sponge kidney i.e. medullary cystic kidney disease

118
Q

What part of the nephron is most affected by amyloidosis?

A

mesangium

119
Q

By how much does effective renal plasma flow underestimate the true renal plasma flow?

A

10%

121
Q

Tx of PSGN

A

resolves spontaneously

123
Q

Why do beta-adrenergic agonists cause hypokalemia?

A

They increase the effectiveness of Na/K ATPases leading to K shift into cells

124
Q

What are you thinking when there is sterile pyuria?

A

urethritis probably

125
Q

What is the most common cause of acute renal failure?

A

acute tubular necrosis (intrarenal azotemia whereby necrotic cells plug up the tubules)

127
Q

What is the most common presenting Sx of renal cell CA?

A

hematuria

128
Q

What receptors are present on JG cells that sympathetic nerves stimulate to increase renin release?

A

Beta 1!!

129
Q

What tumor is comprised of metanephric blastema?

A

Wilms tumor

130
Q

Which tubular cells create the active form of vitamin D under PTH stimulation?

A

PCT cells

132
Q

Why does the thin descending loop of henle make urine hypertonic? Why does the thick ascending limb make it less hypertonic?

A

Thin descending is impermeable to salt, however, water leaves because of the hypertonic medullary interstitium; TALH makes it less concentrated because NKCC is actively reabsorbing salt but this segment is impermeable to water

133
Q

What is the field defect of transitional cell CA?

A

The tendency to recur since the entire urothelium was hit with carcinogens

135
Q

What are the IF findings of minimal change Dz? What is the Tx?

A

NONE; corticosteroids because the damage is mediated by cytokines from CD8 T cells against the RS cells

136
Q

Which nephrotic syndrome would not increase the risk of infection? Why

A

Minimal Change disease because only albumin is lost, not immunoglobulins

138
Q

Discuss how total body water is distributed

A

TBW is 60% of the mass; 2/3 is intracellular, 1/3 is extracellular? Of the extracellular, 3/4 is interstitial and 1/4 is plasma

139
Q

What will you see on light microscopy of focal segmental glomerulosclerosis? Electron microscopy?

A

LM = segmental sclerosis and hyalinosis; EM = podocyte effacement (also in minimal change Dz)

140
Q

Where are the deposits in SLE?

A

DEPENDS!! If it causes nephrotic syndrome then it is subepithelial (membranous nephropathy) if it is nephritic it is subendothelial (DPGN)

142
Q

Why does creatinine mildly overestimate GFR?

A

Some is secreted but mostly just freely filtered

144
Q

What are the major associations of MPGN I and II?

A

I = associated with HBV and HCV; II associated with C3 nephritic factor

145
Q

What effect does increased plasma protein concentration have on 1) RPF 2) GFR 3) FF

A

1) no change 2) decreased 3) decreased

146
Q

What is C3 nephritic factor? Which disease is it associated with?

A

An autoantibody that stabilizes C3 convertase leading to overactivation of complement and it is associated with membranoproliferative glomerulonephritis II

148
Q

How do you differentiate Acute PSGN from membranous nephropathy without clinical Hx?

A

Both have supepithelial granular deposits? However, membranous has GBM thickening and PSGN will be hypercellular

150
Q

What effect does AT II have on baroreceptors and why?

A

It limits reflex bradycardia which would happen normally due to its pressor effect

151
Q

What do granular casts indicate?

A

Acute tubular necrosis (muddy brown)

152
Q

Family history of brain hemorrhages and renal dz

A

ADPKD (PDK gene 1 or 2, chromosome 16)

153
Q

Which MPGN is associated with HBV and HCV?

A

Type I (tram-tracking subendothelial deposits)

154
Q

Diagnosis for renal Bx with LM = hypercellular glomeruli, with neutrophils; EM = subepithelial deposits; IF = granular appearance with IgM, IgG and C3

A

Acute PSGN

155
Q

What are the Tx for calcium stones?

A

Citrate and thiazide diuretics

156
Q

How does the loss of VHL in Von Hippel Lindau lead to tumorigenesis?

A

increases IGF-1 and HIF (a transcription factor) leading to tumorigenesis

157
Q

What is the diagnosis of renal Bx with segmental sclerosis and hyalinosis on LM and podocyte effacement on EM?

A

Focal Segmental Glomerulosclerosis (nephrotic)

159
Q

What paraneoplastic syndromes are associated with renal cell CA?

A

ectopic EPO, ACTH, PTHrP

161
Q

Which glomerulopathy leads to loss of albumin only?

A

Minimal change disease (globulins are not lost)

162
Q

Which structure is anterior to a ureter in a male? Female?

A

Male = vas deferens; Female = uterine artery

163
Q

What if the PCO2 differs significantly from that predicted in the Winter’s formula?

A

There is probably a mixed acid-base disorder

164
Q

Most common tumor of urinary tract

A

Transitional Cell CA

165
Q

What 2 substances may cause calcium oxalate stones?

A

Ethylene glycol (metabolized to oxalate) and Vitamin C (increases oxalate uptake, and iron)

167
Q

What cancer is associated with minimal change disease? Explain

A

Hodgkin lymphoma; classically causes B signs, so the cytokines released directed at RS cells (CD15 and CD30) leads to podocyte effacement

168
Q

Discuss how you can determine what is reabsorbed etc. based on knowing the clearance of a solute and the GFR

A

If clearance is less than GFR something is reabsorbed, if greater, it is secreted? If they are equal there is no net in either way

169
Q

What effect does afferent arteriole constriction have on 1) RPF 2) GFR and 3) FF

A

1) decreased 2) decreased 3) unchanged (FF = GFR/RPF

170
Q

Discuss the statement that acute tubular necrosis is not interchangeable with acute kidney injury

A

Acute tubular necrosis is a form of acute kidney injury. However, AKI may have prerenal and postrenal causes as well. However, the most common cause of AKI intrinsically is in fact, ATN

171
Q

6 causes of hyperkalemia?

A

Digitalis (decreases Na/K), Hyperosmolarity, Lysis of cells, acidosis (exchange for H), Beta-adrengergic antagonists (decreases Na/K)

172
Q

Which syndrome involves Wilms tumor and muscle hemihypertrophy with mutations in WT2 instead of WT1?

A

Beckwith-Weidmann syndrome

173
Q

What is the major risk factor for sporadic renal cell CA? location?

A

smoking; upper pole (yellow mass)

174
Q

Discuss Hartnup disease

A

loss of Na-dependent amino acid transporter of neutral AA’s in PCT. Tryptophan is not reabsorbed so s/s of pellagra because niacin (B3) is from tryptophan

175
Q

7 causes of normal anion gap metabolic acidosis (HARD ASS)

A

Hyperalimentation, Addison’s, Renal tubular acidosis (including Fanconi), Diarrhea, Acetazolamide, Spironolactone, and Saline infusion

176
Q

From what cells does renal cell carcinoma arise?

A

PCT (at least clear cell CA)

177
Q

Painless hematuria with no casts

A

Suggests bladder CA (transitional cell CA)

178
Q

You are at increased risk of what when on dialysis for CKD

A

Renal cell carcinoma

180
Q

What is the key finding in acute tubular necrosis (urinalysis finding)?

A

granular (muddy brown) casts

181
Q

What is renal papillary necrosis?

A

Sloughing of renal papillae leading to gross hematuria and proteinuria associated with SODA (Sickle cell, obstructive pyelonephritis, DM, and analgesics (chronic phenacetin))

182
Q

Name 2 Dz with mixed nephritic and nephrotic findings

A

Diffuse proliferative glomerulonephritis, Membranoproliferative glomerulonephritis

183
Q

Which casts are seen in acute cystitis?

A

No casts, just pyuria; casts only in pyelonephritis

184
Q

If you suspected urate stones how would you visualize them? Who gets them?

A

Ultrasound and CT can visualize but NOT X-Ray; Gout pts and ppl being Tx’d for leukemia (tumor lysis syndrome)

185
Q

What is the main concern of an angiomyolipoma aside from the fact that it is associated with tuberous sclerosis?

A

spontaneous rupture (retroperitoneal bleed)

186
Q

What do oval fat bodies in urine suggest?

A

Nephrotic syndrome (fatty casts)

187
Q

Name 6 toxic agents that can cause acute tubular necrosis

A

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

189
Q

What is the classic urine finding in acute pyelonephritis?

A

WBC casts

190
Q

5 associations of Focal Segmental Glomerulosclerosis

A

HIV (collapsing variant), Heroin abuse, Massive obesity, IFN Tx (i.e. Kaposi, HBV, HCV, MS), and CKD d/t either surgical removal or congenital loss

191
Q

What is the nephrotic presentation of SLE? Nephritic? Which kills?

A

Nephrotic is membranous nephropathy; Nephritic is Diffuse Proliferative glomerulonephritis (#1 cause of death in SLE)

192
Q

What hormone may act as a “check” on the RAAS?

A

ANP which is essentially the physiologic antagonist of AT II

193
Q

What is the cause of nephrotic syndrome with LM findings of mesangial expansion, GBM thickening, and eosinophilic nodular glomerulosclerosis?

A

Non-Enzymatic Glycation of GMB i.e. these are Kimmelsteil Wilson nodules of diabetic nephropathy

194
Q

Name 4 causes of K shifting into cells

A

Hypo-osmolarity, insulin (increases Na/K ATPase), Alkalosis (exchange for H), and beta-adrenergic agonists (increase Na/K fxn)

195
Q

Which arteriole is more affected by diabetic nephropathy?

A

efferent (leads to hyperfiltration injury)

196
Q

Do most people develop chronic pyelonephritis?

A

NO, there is usually a predisposing factor such as vesicoureteral reflux or chronic obstructing kidney stones

197
Q

What gene and chromosome are affected in Wilm’s tumor? What syndrome is it associated with?

A

WT1 gene on chromosome 11; Beckwith-Weidmann syndrome

198
Q

Name 4 strictly nephritic syndromes

A

PSGN, Rapidly progressive glomerulonephritis, Berger’s IgA nephropathy, Alport Syndrome

PATHOMA/FA SYSTEMS (10 decks)

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