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Med Phys > Kidney Pathophysiology > Flashcards

Kidney Pathophysiology Flashcards

1
Q

Acute renal failure

A

Kidneys abruptly stop working with rapid decline in GFR.

Causes rapidly developing BUN, creatinine, and electrolyte imbalance.

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2
Q

Chronic renal failure

A

Progressive loss of kidney function.

Causes same effects as acute renal failure but developing over time.

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3
Q

What are the three general categories which kidney disease is initiated in?

A
  1. Large blood vessels supplying the kidney or vessels of the body overall
  2. Glomeruli, tubules, renal interstitium
  3. Parts of the urinary tracts outside the kidneys.
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4
Q

Prerenal Renal failure

A

Decreased blood supply to the kidney

Due to a cause external to kidneys, such as heart failure, severe hemorrhage, severe decrease in blood pressure, renal artery stenosis

Occurs when renal blood flow is reduced to <20% of normal –> this is the point at which cells become hypoxic due to low oxygen.

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5
Q

Intrarenal Renal failure

A

Abnormality in the kidney itself.

Due to damage to blood vessels of the kidney, to the tubular epithelial cells, or to the renal interstitium

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6
Q

Postrenal renal failure

A

Obstruction of the urinary collecting system.

If BOTH kidneys have distal obstruction, then backup of urine into the kidneys can lead to kidney damage.

If it is just to one kidney then the other can increase urine output to compensate.

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7
Q

Oliguria

A

Diminished urine output below level of intake of water and solutes leading to accumulation of water and solutes in the body fluids.

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8
Q

Possible etiologies of prerenal acute renal failure

A
  1. ECF volume decrease (hemorrhage, vomiting, diarrhea, large burns)
  2. Cardiac failure
  3. Hypotension (shock, anesthesia, renal artery stenosis)
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9
Q

Possible etiologies of intrarenal acute renal failure

A
  1. Conditions that injure the glomerular capillaries (malignant HTN, vasculitis, acute glomerulonephritis)
  2. Conditions that damage the renal tubular epithelium (renal tubular necrosis due to ischemia or toxins)
  3. Conditions that cause damage to the renal interstitium.
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10
Q

Possible etiologies of postrenal acute renal failure

A
  1. Bilateral obstruction of the ureters or renal pelvis by large kidney stones or blood clot
  2. Bladder obstruction
  3. Obstruction of the urethra
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11
Q

What is the biggest acute threat of acute renal failure?

A

Hyperkalemia – Injury to the tubule and deposition of casts makes secretion of electrolytes difficult.

Increase of even 4 mEq/L can be fatal.

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12
Q

Physiologic effects of acute renal failure

A
  1. Retention of water and electrolyes
  2. Hyperkalemia
  3. High concentration of non-protein nitrogens in ECF (uremia, azotemia)
  4. Metabolic acidosis
  5. Death within 8-14 days if no treatment.
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13
Q

Vicious cycle of chronic renal failure

A

Progressive injury of functional nephrons –> Leads to sclerosis of the glomerulus which further decreases kidney function.

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14
Q

What are the most common etiologies of CKD in developed nations?

A
  1. DM
  2. HTN
  3. Glomerulonephritis
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15
Q

Common etiologies of pre-renal CKD

A

Atherosclerosis of large vessels

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16
Q

Common etiologies of intrarenal CKD

A

Diabetes mellitus/obesity/metabolic syndrome
Hypertension; nephrosclerosis
Glomerulonephritis – e.g. local or systemic (polyarteritis nodosa, SLE) causes
Nephrotic syndrome disorders
Infections
Nephrotoxins
Polycystic kidney disease (genetic)

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17
Q

Common etiologies of postrenal CKD

A

Urinary tract obstructions -calculi, BPH, urethral constriction

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18
Q

What happens to the function nephrons in a person with CKD?

A

Increased blood flow, increased reabsoprtion, and hypertrophy

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19
Q

Additional effects of CKD

A

Anemia – due to decreased erythropoietin secretion by kidneys
Neuropathy – cognitive and neuromuscular due to uremia
Osteomalacia – bones are partially absorbed
due to less active vitamin D formation . Vitamin D is activated by 2 steps: liver then kidney
Accumulation of phosphate due to decreased GFR
Phosphate binds with Ca2+ leaving less ionized Ca2+ in the serum, stimulating PTH secretion, causing bone resorption
Heart failure, pulmonary edema
Increased half-life of insulin

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20
Q

What are the two main categories of renal vascular disease?

A
  1. Renal artery stenosis

2. Nephrosclerosis

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21
Q

Renal artery stenosis

A

Either narrowing due to atherosclerotic plaque or fibromuscular dysplasia.

Systemic HTN occurs secondary to RAS (activation of renin angiotension system to hold on the Na and Water –> increased blood pressure.)

Affected kidney shows diffuse atrophy and same effect of increased GFR to healthy kidney.

22
Q

Nephrosclerosis

A

Associated with HTN and hardening and decrease in function of nephrons.

Medial and intimal thickening with hylinization of arteriolar walls which narrows the vessel lumens.

Causes ischemia and damage to the kidney and leakage of plasma.

23
Q

Malignant nephrosclerosis

A

Widespread kidney damage due to extreme HTN and eventual ischemia.

This is a medical emergency that requires immediate treatment.

24
Q

Renal vascular disease- Thrombotic microangiopathies

A

Spectrum of clinical syndromes characterized by excessive activation of platelets which deposit as thrombi in capillaries and arterioles of kidney and other organs.

Thrombi cause turbulence which shears RBCs, leading to microangiopathic hemolytic anemia (circulating fragmented RBCs (schistocytes) resulting from fragmentation as the erythrocyte as they flow through injured small vessels

Includes: Thrombotic thrombocytopenic purpura
and hemolytic-uremeic syndrome

25
Q

Tubulointerstitial nephritis

A

Group of renal diseases with inflammatory injuries to tubules and interstitium.

Characterized by azotemia (not able to filter out urea or other proteins) without nephritic or nephrotic syndrome.

Ex: Pyelonephritis, drugs toxins, and metabolic diseases

26
Q

Pyelonephritis

A

Inflammation of tubules, interstitium, and renal pelvis due to infection.

Acute or chronic

Usually caused by gram negative bacilli from the intestinal tract.

Affects the renal medulla first —> impaired ability to concentrate urine

27
Q

Tubulointerstitial nephritis: Drugs and toxins

A

Mechanisms:
1. direct tubular injury
trigger of interstitial immune reaction
2. Drugs modify an extracellular component of a tubular epithelial cell, which becomes immunogenic.

28
Q

Polycystic kidney disease

A

A hereditary disorder characterized by multiple expanding cysts of both kidneys that eventually destroy renal parenchyma and cause renal failure.

29
Q

Urolithiasis

A

Stone precipitation in urinary tract due to supersaturation of constituents.

Types: Calcium stones (most common)
Uric acid stones
Triple stones
Cysteine stons

30
Q

Urolithiasis clinical features

A

Pain due to distention of ureter, renal pelvis or renal capsule. Sometimes there will be hematuria.

31
Q

Glomerular disease patterns

A
  1. Nephrotic

2. Nephritic

32
Q

Nephrotic syndrome

A

Loss of large quantities of plasma protein in urine due to increased permeability of the glomerular membrane.

Massive proteinuria
Low serum albumin
Peripheral edema
Hyperlipidemia and lipiduria
Thrombotic disease
33
Q

Nephritis syndrome

A

Caused by inflammation in the glomeruli.

Hematuria
Renal insufficiency 
oliguria 
Mild to moderate HTN
Mild proteinuria
34
Q

What are the 4 pathologic mechanisms of glomerular injury?

A
  1. Hypercellularity (proliferation of messangial, endothelial, or endothelial cells with infiltration of leukocytes)
  2. Basement membrane thickening (deposition of material usually immune complexes)
  3. Hyalinosis (Accumulation of extracellular eosinophilic material that has leaked from capillaries)
  4. Sclerosis (accumulation of extracellular collagenous matrix)
35
Q

Most types of primary and secondary causes of glomerular injury are _______ mediated

A

Immune

Can be antibody-mediated or cell-mediated injury

36
Q

Nephrotic syndrome pathology

A

Usually the podocyte is the site of injury and often these is no gross inflammation present with light microscopy.

Possible features: Effacement of foot process, deposition of immune complexes in the GBM.

37
Q

Result of loss of protein (hypoalbuminemia) in the kidney

A

Edema
Decreased intravascular volume (low BP)
RAA activated and ADH elevated
Hyperlipidemia
Hypercoagulability
Increased susceptibility to infections due to IgG loss
Vitamin D and thyroid hormone deficiency due to loss of proteins that bind these factors.

38
Q

Minimal change disease

A

Most common cause of idiopathic nephrotic syndrome in children.

Histology usually shows effacement of foot processes on electron microscope that is thought to be mediated by cytokines from T cells that damage podocytes.

Highly selective proteinuria: Size selectivity still remains.

It is usually non-progressive and most children respond well to corticosteroids.

39
Q

Focal segmental glomerulosclerosis

A

Injury to epithelial cells can be an initiating cause (putative circulating factor that cause dysfunction, known podocyte mutations, drugs)

Or.. overwork of glomeruli can be the initiating cause (compensatory hypertrophy due to decreased amount of functional renal tissue or obesity).

Can see segmental sclerosis and hyalinosis in some glomeruli but extensive effacement of podocyte foot processes

Tubular atrophy in affected glomeruli.

40
Q

Membranous glomerulonephropahty

A

Most common cause of idiopathic nephrotic syndrome in adults. Causes nonselective proteinuria. Variable in how the disease progresses –> HTN (30%), spontaneous remission (20%) and progressive renal failure (30-40%)

Diffuse thickening of the glomerular basement membrane due to deposits of immune complex- IgG along the subepithelial side of the BM.

Can be idiopathic (primary) or secondary due to associated with other autoimmune diseases, drugs, tumors, and infections.

Can see granular IgG deposits in the basement membrane with immunofluorescence.

41
Q

Membranoproliferative glomerulonephritis

A

Disorder that can present with nephrotic and or nephritic syndrome and involves deposition of factors in GBM.

Clinical features are mixed nephrotic and nephritis and include hypocomplementemia and slow progressive onset (for most)

Histology shows proliferation of endothelial cells and mesangial cells as well as duplicated GBM (tramtracks)

42
Q

Membranoproliferative glomerulonephritis (MPGN) major histologic types

A

Immune complex mediated (IgG+ complement) Type 1
This is the most common type and is usually see in disease states where there is chronic infection and inflammation (Hep C)

Complement-mediated MPGN (Type II) Less common and is due to abnoesrmal activation of alternative complement pathway.

43
Q

Diabetic nephropahty

A

Syndrome occurring due to diabetes-mediated kidney damage.

Usually presents initially as sub-nephrotic range proteinuria (microalbuminuria), but with eventual progressive decline in glomerular filtration rate and hypertension and nephrotic range proteinuria

Diffuse glomerulosclerosis
Expansion of the mesangial matrix with ECM mesangial sclerosis

44
Q

What are Kimmelstiel-Wilson nodules

A

Can be present in diabetic nephropathy.

Well-defined nodules due to expansion of the mesangial matrix with EMC mesangial sclerosis.

45
Q

Immunoglobulin A (IgA) Nephropathy (Berger Disease)

A

Most common primary glomerular disease worldwide (less common in US)

Characteristic synpharyngitic presentation- onset of features at the same time as the onset of URTI.

Clinical features: hematuria, subnephrotic proteinuria, HTN, and renal insufficeincy.

Aberrantly glycosylated IgA deposited in mesangium of glomeruli –> proliferation of messangial cells and inflammation.

Main histological finding of messangial dense deposits.

46
Q

Post-streptococcal glomerulonephritis

A

Often seen after pharyngitis or impetigo. Classic acute nephritis, hematuria, pyuria, RBC casts, edema, HTN, and oliguric renal failure. Usually acute and recovers in a few weeks but can rarely progress to RPGN.

Anti-M (bacterial cell wall protein) antibody complexes get stuck in the glomerular basement membrane.

Mesangial cells between endothelium and epithelium proliferate and WBCs become entrapped in the glomeruli. Blockage or increased permeability of the glomerulus.

Histology shoes marked glomerular hypercellularity and proliferation of endothelial and mesangial cells.

47
Q

Rapidly progressive glomerulonephritis

A

Severe form of glomerulonephritis with formation of cresents due to proliferation of the epithelial cells lining Bowman’s capsule and inflammation.

In severe rapidly progressing forms scaring can lead to CKD and ESRD in weeks to months.

Can be caused by: Anti-GBM antibodies, Immune complex deposition disorders, pauci-immune RPGN (ANCAs)

48
Q

RPGM: Crescents

A

Mass of proliferating epithelial cells and leukocytes in Bowman’s capsule intermixed with fibrin. Can be due to rupture of the GBM.
(Stuff in the capillary is being squished down by the build up of proliferating epithelial cells in the crescent shape.

49
Q

Renal cell carcinoma

A

Tobacco is the largest risk factor. Tendency to metastasize w/o symptoms.

Can be classified as clear cell carcinoma (cells with clear granular cytoplasm) or papillary carcinoma (papillary growth pattern)

50
Q

Wilms tumor

A

Most common primary renal tumor of childhood.

Tumors resemble cell types which recapitulate developmental stages of the kidney.

Med Phys (4 decks)

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