Renal - Pathology

shaile's version from 2015-05-06 21:06

Misc. Pathologies

Question Answer
RBC casts are sign of glomerulonephritis, ischemia, or malignant hypertension
WBC casts are sign of tubuiointerstltiaI inflammation, acute pyelonephritis, transplant rejection.
Presence of casts indicatesthat hematuria/pyuria is of renal origin
Granular ("muddy brown" ) casts indicateacute tubular necrosis
Waxy casts indicateadvanced renal disease/CRF
Hyaline casts indicatenonspecific
RBCs in urine w/ no casts indicateBladder cancer, kidney stones
WBCs in urine w/ no casts indicateAcute cystitis
Kidney stones complicationshydronephrosis and pyelonephritis
Kidney stone treatment & preventionfluid Intake
Ca kidney stonesMost common kldney stones. Calcium oxalate, calcium phosphate, or both.
From conditions that cause hypercalcemia (cancer, ↑ PTH, ↑ vitamIn D, milk-alkali syndrome) can lead to hypercalciuria and stone---- pt= hypercalciuria, normocalcemia
Tend to recur. Tx w thiazides and citrate (and hydration)
Ca-oxalate stonesppt @ ↓ pH
can result from ethylene glycol or vitamin C abuse, malabsorption w/ Crohn's
Ca-phosphate stonesppt @ alkaline pH, radiopaque
Ammonium magnesium phosphate (struvite) kidney stones2nd most common kidney stone. Caused by infection with urease-positive bugs (Proteus vulgaris, Staphylococcus, Klebsiella ).
Can form staghorn calculi that can be a nidus for UTls.
Radiopaque - ppt in alkaline pH
Uric acid stonesassociation with hyperuricemia (e .g., gout). Often seen as a result of diseases with ↑ cell turnover, such a leukemia and myeloproliferative disorders. RadiolUcent, ppt in acidic pH
Cystine kidney stonesMost often secondary to cystinuria
Hexagonal shape
Faintly radiopaque, ppt in acidic pH
Treat with alkalinzation of urine
Acute pyelonephritisAffects cortex with relative sparing of glomeruli/vessels. WhIte cell casts in urine are classic. Presents with fever, CVA tenderness, nausea, and vomiting
neutrophilic infiltrate
Acute pyelonephritis bugsE.coli = #1(fimbriae, pili), Proteus (urea splitter), Klebsiella (urea splitter), Enterococcus faecalis (- on nitrite dipstick)
Chronic pyelonephritisCoarse, asymmetric corticomedullary scarring, blunted calyx, Tubules can contain eosinophilic casts (thyroidization of kidney)
lymphocyte invasion
What predisposes a pt to chronic pyelonephritis developmentvesicoureteral reflux
chronically obstructing kidney stones
or another disorder that predisposes the pt to recurrent infections
Drug-induced interstitial nephritisAcute interstitial renal inflammation. Pyuria (typically eoslnophlls) and azotemia occuring 1- 2 weeks after admin.
Associated with fever, rash, hematuria, and CVA tenderness.
Drugs (e.g., diuretics, NSAIDs, penicillin derivatlves, sullfonamides, rifampin) act as haptens, Inducing hypersensitivity
Diffuse cortical necrosisAcute generalized infarction of cortices of both kidneys. Likely due to a combination of VASOSPAM and DIC. Associated with obstetric catastrophes (e.g., abruptio placentae) and septic shock.
Acute tubular necrosisMost common cause of acute renal failure in hospItal. Self-reverslble, but fatal if left untreated (provide supportive dialysis).
Associated with renal ischemia (e.g., shock, sepsis), crush injury (myoglobulinuria), toxins.
Death most often occurs during initial oliguric phase
Loss of cell polarity, epithelial cell detachment, necrosis
granular ("muddy brown") casts
Stages of Acute tubular necrosis3 stages: inciting event→ maintenance (low urine w/ risk of hyperkalemia) → recovery (2-3 weeks) w/ polyuria and risk of hypokalemia
Renal papillary necrosisSloughing of renal papillae → gross hematuria, proteinuria. May be triggered by recent infection or immune stimulus.
Associated with :1. Diabetes mellitus 2. Acute pyelonephritis 3. Chronic phenacetin use (acetaminophen is phenacetin derivative) 4. Sickle cell anemia
Acute renal failure (acute kidney injury)an abrupt decline in renal function with ↑ creatinine and ↑ BUN over a period of several days.
Prerenal azotemia↓ RBF (e.g., hypotension) →↓, GFR. Na+/H2O and urea retained by kidney, so BUN/creatinine ratio ↑ in attempt to conserve volume
Intrinsic renal failuredue to acute tubular necrosis or ischemia/toxins; less commonly due to acute glomerulonephritis (e.g., RPGN).
Patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule → ↓ GFR.
Urine has epithelial/granular casts.
BUN reabsorption is impaired → ↓BUN/creatinine ratio
Postrenal failure outfow obstruction (stones, BPH, neoplasia, congenital anomalies). Develops only with bilateral obstruction.
Prerenal azotemia labsUrine osmolality (>500), Urine Na (<20), FeNa(<1%), Serum BUN/Cr(>20)
Intrinsic renal failure labsUrine osmolality (<350), Urine Na(>40), FeNa(>2%), Serum BUN/Cr(<15)
Postrenal failure labsUrine osmolality (<350), Urine Na (>40), Fe(>4%), Serum BUN/Cr (>15)
Consequences of renal failure1. Na+/H2O retention (CHF, pulmonary edema, hypertension)
2. Hyperkalemia
3. Metabolic acidosis
4. Uremia-clinical syndrome
5. Anemia (failure of EPO production)
6. Renal osteodystrophy (failure of vitamin D hydroxylation)
7. Dyslipidemia (especially ↑ triglycerides)
8. Growth retardation and developmental delay (in children)
Uremia-clinical syndrome ↑ BUN and ↑ creatinine, Nausea and anorexia, Pericarditis, Asterixis, Encephalopathy, Platelet dysfunction
Renal osteodystrophyfailure of vit D hydroxylation --> Ca2+ wasting & PO4 retention --> 2° to hyperparathyroidism
Causes subperiosteal thinning of bones
Fanconi’s syndrome↓ proximal tubule transport of amino acids, glucose, phosphate, uric acid, protein, and electrolytes.
Can be congenital or acquired.
Causes include Wilson's disease, glycogen storage diseases, and drugs (e.g., tenofovir, expired tetracycline), ischemia, multiple myeloma
Defects - ↓phosphate reabsorption, ↓HCO3 reabsorption, ↓early Na+ reabsorption
Complications - Rickets, Metabolic acidosis (type II RTA), ↑ distal Na+ reabsorption→hypokalemia

Glomerular Diseases

Question Answer
Nephritic syndromean Inflammatory process. when it involves glomeruli, it leads to hematuria and RBC casts in urine. Associated with azotemia, oliguria, hypertension,and proteinuria < 3.5 g/day).
Acute poststreptococcal glomerulonephritis LMLM:glomeruli enlarged and hypercellular, neutrophils, “lumpy-bumpy" appearance
Acute poststreptococcal glomerulonephritis EM & IFNephritic, subepithelial immune complex (IC) humps.
Acute poststreptococcal glomerulonephritis IFgranular appearance d/t IgG, IgM, and C3 deposition along GBM and mesangium
Acute poststreptococcal glomerulonephritis notesnephritic
Presents as: kids with facial edema, dark (coca-cola) urine, and hypertension following group A strep infxn of skin (3 weeks) or pharynx (2 weeks)
Group A Strep--- M protein, ASO antigen
Increased anti-DNase B titers
Decreased complement
Resolves spontaneously
Rapidly progressive (crescentic) glomerulonephritis (RPGN) LM and IFcrescent-moon shape. Crescent consists of fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes, and macrophages
Rapidly progressive (crescentic) glomerulonephritis (RPGN) diseasesNephritic
1. Goodpasture’s (hematuria and hemoptysis)
2. Wegener’s granulomatosis (granulomatosis w polyangiitis) (c-ANCA)
3. Microscopic polyarteritis (p-ANCA)
Goodpastures syndromeNephritic (RPGN) disease
Male dominant - HLA-DR2 positive
Type II hypersensitivity Ab against GBM & alveolar membrane (linear IF) resulting in hematuria/hemoptysis
Wegener’s granulomatosisNephritic RPGN (c-ANCA), necrotizing granulomas, affects renal & upper airway
Microscopic polyarteritisNephritic RPGN (p-ANCA), no granulomas
Diffuse proliferative glomerulonephritisNephritic
Subendothelial DNA-anti-DNA ICs - activate classical complement pathway
Wire looping of capillaries & neutrophil infiltration with hyaline thrombi in capillary lumens
Granular IF
Develops into CRF → most common cause of death in SLE (can also be d/t MPGN)
Berger’s disease (IgA glomerulonephropathy)Nephritic
Most common nephropathy
↑ synthesis of IgA
LM and IF - ICs deposit in mesangium & mesangial proliferation - ICs activate alternative complement pathway
Often presents with episodic bouts of hematuria following URIs and HTN
Alport’s syndromeNephritic
Mutation in α-chains (3,4,5) of type IV collagen→split basement membrane
Glomerulonephritis, nerve disorders, deafness, ocular disorders
X-linked recessive
Nephrotic syndromeNephrotic syndrome present. with massive proteinuria (> 3.5g/day, frothy urine), hyperlipidemia, fatty cast, edema. Associated with thromboembolism and ↑ risk of infection (loss of immunoglobulins).
Membranous glomerulonephritis (diffuse membranous glomerulopathy)Nephrotic
LM - diffuse capillary and GBM thickening.
EM Silver stain shows "spike and dome" appearance with subepithelial deposits.
IF - granular. SLE's nephrotic presentation
Membranous glomerulonephritis (diffuse membranous glomerulopathy) causeDrugs (captopril, gold therapy)
Infections: HBV, malaria, syphilis
Cancer: lung/colon carcinomas, Hodgkin's lymphoma
Minimal change disease (lipoid nephrosis)Nephrotic
LM - normal glomeruli
EM - foot process effacement by t-cell cytokines - selective loss of albumin, not globulins, due to GBM polyanion loss
Most common in children. - May be triggered by a recent infection or an immunization
Responds to corticosteroids.
LM - congo red stain, apple-green birefringence
Associated with multiple myeloma, chronic conditions, TB, RA
Diabetic glomerulonephropathyNephrotic
Nonenzymatic glycosylation (NEG) of GBM → ↑ permeability, thickening
NEG of efferent arterioles ↑GFR → mesangial expansion
LM- mesangial expansion, GBM thickening, nodular glomerulosclerosis (Kimmelstiel-Wilson lesion)
Focal segmental glomerulosclerosisNephrotic
LM-segmental sclerosis and hyalinosis
EM-focal damage to visceral epithelial cells
Most common glomerular disease in HIV patients and IV heroin users - more severe in HIV patients
Most common cause of adult nephrotic syndrome
Membrano-proliferative glomerulonephritis Type 1Nephrotic & Nephritic
Subendothelial lCs with granular IF.
EM- “tram-track" appearance due to GBM splitting caused by mesangial ingrowth.
Associated with HBV, HCV
Presents with HTN and hematuria
Membrano-proliferative glomerulonephritis Type IINephrotic & Nephritic
EM- Intramembranous IC deposits; "dense deposits"
HTN and hematuria - usually progresses slowly to CRF
Type II assoc w/C3 nephritic factor - binds to C3 convertase and sustains activation of C3 → very low C3 levels
Causes of chronic glomerulonephritisRPGN
Focal segmental glomerulosclerosis
Type 1 membranoproliferative glomerulonephritis
Membranous glomerulopathy
Type 4 diffuse proliferative glomerulonephritis in SLE
IgA glomerulopathy

Picture Quiz - Glomerular diseases

Renal - Picture Quiz - Glomerular diseases (by bri1231)

Cysts & Tumors

Question Answer
Renal cell carcinoma pathoOriginates in renal tubular cells → polygonal clear cells. Manifests clinically with hematuria, palpable mass, 2° polycythemia, flank pain, fever, and welght loss.
Renal cell carcinoma associationsvon Hippel-Lindau and gene deletion in chromosome 3
paraneoplastic syndromes (ectopic EPO, ACTH, PTHrP, prolactin)
Renal cell carcinoma epidemiologyMost common renal malignancy, Most common in men ages 50-70. ↑ incidence with smoking and obesity.
Renal cell carcinoma complicationsInvades IVC and spreads hematogenously; metastasizes to lung, bone
Wilm’s tumor (nephroblastoma)Most common renal malignancy of early childhood (ages 2- 4), Contains embryonic glomerular structures
Wilm’s tumor (nephroblastoma) sxshuge, palpable flank mass and/or hematuria
Wilm’s tumor (nephroblastoma) associationsDeletion of tumor suppressor gene WTI on chromosome 11. Can be part of WAGR complex: Wilms' tumor, Aniridia (absence of iris), Genitourinary malformation , and mental-motor Retardation
Beckwith-Wiedman Syndrome = hemi-hypertrophy - 1 side grows faster than the other
Transitional cell carcinomaMost common tumor of urinary tract system (can occur In renal calyces, renal pelvis, ureters, and bladder)
Transitional cell carcinoma sxsPainless hematuria w/o casts is suggestive of bladder cancer
Transitional cell carcinoma associations"problems in your Pee SAC": Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide
Transitional cell carcinoma histopapillary growth lined by transitional epithelium w/ mild nuclear atypia & pleomorphisms
Squamous cell carcinoma of bladderShistomiasis. Haematobium = blood fluke; see keratin pearls
ADPKDMultiple, large, bilateral cysts that destroy the parenchyma. Enlarged kidneys
ADPKD sxsflank pain, hematuria, hypertension, urinary infection, progressive renal failure, Death from complication of chronic kidney disease or hypertension (due to ↑ renin production).
ADPKD associationsAutosomal-dominant mutation in APKDl or APKD2 (chr. 16). Associated with polycystic benign hepatic cysts, berry aneurysms, mitral valve prolapse
ARPKDInfantile presentation in parenchyma, enlarged kidney w/ smooth surface w/ cysts arranged in rows causing dilating of collecting tubules
ARPKD associationsAutosomal recessive. Associated with congenital hepatic fibrosis.
Significant renal failure in utero can lead to Potter's
Concerns beyond neonatal period are hypertension, portal hypertension, and progressive renal insufficiency
Dialysis cystsCortical and medullary cysts resulting from long-standing dialysis; RCC over 10 yrs of dyalsis; cysts contain oxalate crystals
Simple cysts Benign, incidental finding. Cortex only.
Medullary cystic diseaseThese cysts sometimes lead to fibrosis and progressive renal insufficiency with urinary concentrating defects. Ultrasound shows small kidney. Poor prognosis