10/23

Question 1

AKI definition and classification

Answer 1

• loss of function (decline in GFR) developing over hours-days
• clinically, acute rise in PCr
• class: pre-renal, renal, post-renal, vascular/NOS

Question 2

Prerenal AKI (etiologies, pathophys, labs,)

Answer 2

• etiologies: volume (hemorrhage, GI, etc), CO (CHF, MI, PE), low SVR (sepsis, liver failure), high RVR (renal arterial stenosis, liver failure, NSAIDS, calcineurin inhibitors, thrombosis)
• pathophys: below 50-60 mmHg, autoregulation of perfusion fails and afferent arteriole vasoconstricts (worsened by NSAIDs). Restoration of flow usually fixes, but if prolonged can get cell damage and ATN.
• labs: BUN:Cr > 20:1, FeNa < 1UNa < 20, FeUrea <35%, high SG, bland sediment, few hyaline casts

Question 3

Renal/Intrinsic AKI etiologies and urine

Answer 3

• gloms: Acute glomerulonephritis
• Tubes (ATN – muddy-brown/granular casts): ischemic – hypovolemia, cardio shock, septic shock or Nephrotoxic – aminoglycosides, radiocontrast, myoglobin, acute gout
• Interstitial: Rx Reaction (analgesics/NSAIDS, Abx/Cephalosporins, penicillins)–eosinophils!
• Vascular: Emboli, microangiopathies, HUS
• granular and epithelial casts (ATN)
• proteinuria/hematuria with dysmorphic RBCs (GN), WBC casts (AIN)

Question 4

ischemic ATN (cause, pathophys, pathn, natural history, labs, natural history

Answer 4

• subset of AKI (tubular)
• cause: severe/prolonged hypoperfusion
• pathophys: paradoxical afferent arteriole constriction; ischemic endothelial injury/leukocyte activation, epithelial cell injury (loss of polarity, brush border); tubular occlusion –> drop in GFR; inflammation due to cytokines (other organs too!)
• path: focal loss of tubular epithelial cells and cell debris. muddy-brown granular casts on urinalysis
• labs: FENa > 1%, FeUrea >35%
• natural history: full recovery possible (surviving epithelial cells de-differentiate, migrate, proliferate, redifferentiate). Can have partial recovery, or progress to CKD and ESRD

Question 5

postrenal AKI (etiologies, pathophys, imaging, urine)

Answer 5

• etiologies: stone, prostate, neoplasm, neurologic (diabetes), anatomical
• pathophys: decreased GFR from increase tubular pressure and renal vasoconstriction. acutely, increased Na and H2O reabsorption; chronically, Na reabsorption and K/H secretion decreases.
• imaging: hydronephrosis!
• urine: bland sediment

Question 6

Tx AKI

Answer 6

• supportive: optimize volume, BP, treat infection, nutrition, dialysis if necessary.
• specific treatment of etiology.

Question 7

Acute Interstitial nephritis (causes, clinical, path)

Answer 7

• causes: penicillin, dilantin, NSAIDs, omeprazole. also infection etc
• clinical: fever, skin rash, urine eosinophils, PMNs, proteinuria, hematuria, creatinine
• Path: edema and lymphos/plasma/eosinophils in infiltration. some tubulitis. may have granuloma

Question 8

analgesic abuse nephropathy (epi, pattern of injury, path, complications, DDx)

Answer 8

• less common now that penacetin discontinued
• drug-induced TIN
• papillary necrosis (pale papillae with hyperemic border and thinned out overlying cortex)
• DDx: diabetes, sickle cell
• complications: renal failure (can cause obstruction), urothelial carcinoma

Question 9

Hyperuricemia

Answer 9

-acute: purine excess from chemo, muscle breakdown. Urate accumulates and crystallizes, causing obstruction and dilation with ATN

• chronic: deposition of crystals, fibrosis, inflammation, giant cells.
• Saturnine: form of chronic due to lead poisoning of PT cells and failure to excrete urate.

Question 10

nephrocalcinosis (pathophys, common causes, path)

Answer 10

• altered Ca balance –> deposition of crystals in renal parenchyma
• causes: hyperPTH, vit D intox, mets to bone, multiple myeloma
• path: Ca in epithelial cells –> TBM thickening and calcification –> glomerular thickening and Ca crystals in lumen

Question 11

Oxalate nephropathy (causes, path)

Answer 11

• primary (AR mutx) or fat malabsorption, ethylene glycol, excessive intake of oxalate foods.
• path: deposition of crystals in tubular lumen with dilation and atrophy of tubular epithelial cells

Question 12

acute pyelonephritis (types, path)

Answer 12

• ascending (most likely) = interstitial edema and PMNs in interstitium and tubular lumen
• hematogenous (often occurs with preexisting obstruction) = microabscess formation (visible on kidney)
• commonly have inadequate tunneling of ureter through muscular wall
• compound papillae most susceptible

Question 13

Chronic pyelonephritis (causes, path

Answer 13

• repeated episodes of acute PN or xanthogranulomatous PN (massive infiltration of MPhages with some PCs and lymphos. Can look like a mass w/i kidney. inability to clear acute PN.)
• Pathology: irregular cortical scarring, chronic tubular and interstitial inflammation and fibrosis, distortion of the calyces. Thyroidization. Germinal centers(!)

Question 14

Sarcoidosis

Answer 14

immune mediated.
chronic waxing and waning of granulomas
-path: well circumscribed granulomas with NO necrosis

Question 15

IgG4 disease

Answer 15

• excess of IgG4 and mass formation (various organs)

- path: dense masses of “whirling” fibrosis with plasma cell infiltration

Question 16

Paraprotein-mediated damage

Answer 16

• seen in multiple myeloma and other neoplasms
• antibody-like protein deposits in various tissues
• “fractured” casts of paraprotein
• can crystalize w/i epithelial cells