Pathology: Kidneys thru Vascular Diseases (906-956)

Clinical Manifestations of Renal Diseases

• Kidney diseases usually divided into glomeruli, tubules, interstitium, and blood vessels
◦ Glomerular usually immuno
◦ Tubular/interstitium usually toxic/infectious agents
• Azotemia = biochemical abnormality, elevated BUN and creatinine, decreased GFR
• Uremia = azotemia + clinical symptoms (such as.....)
◦ Nephritic syndrome: visible hematuria, mild/moderate proteinuria, HTN. **classic
presentation of acute poststreptococcal glomerulonephritis
◦ Rapidly progressive glomerulonephritis: nephritic syndrome + rapid decline in GFR
◦ Nephrotic syndrome: heavy proteinuria, hypoalbuminemia, severe edema, hyperlipidemia,
and lipiduria
◦ Asymptomatic hematuria or proteinuria
◦ Acute renal failure: oliguria or anuria, recent onset of azotemia
◦ Chronic renal failure: prolonged symptoms/signs of uremia
◦ Renal tubular defects: polyuria, nocturia, electrolyte disorders
◦ UTI: bacteriuria and pyuria (leukocytes in urine); may affect kidney or bladder
◦ Nephrolithiasis: renal colic and hematuria
• Stages from normal kidneys to symptomatic chronic renal failure:
1. Diminished renal reserve: GFR = 50%, other values normal, no symptoms, more
susceptible to azotemia
2. Renal insufficiency: GFR = 20-50%, azotemia appears, anemia, HTN, polyuria and
nocturia can occur
3. Chronic renal failure: GFR under 20%, edema, metabolic acidosis, hyperkalemia,
neuro/GI/cardio complications
4. End-stage renal disease: GFR under 5%
Glomerular Diseases
• Primary and secondary glomerular diseases can look the same clinically and histologically
• Clinical Manifestations
◦ Patients with glomerular disease should also be checked for SLE, diabetes, vasculitis,
amyloidosis
◦ The Glomerular Syndromes:
▪ Nephritic syndrome
▪ Rapidly progressive glomerulonephritis
▪ Nephrotic syndrome
 ▪ Chronic renal failure
▪ Isolated urinary abnormalities
• Histologic Alterations
◦ Various glomerulopathies characterized by one or more of 4 basic tissue reactions:
▪ Hypercellularity
• Cellular proliferation of mesangial or endothelial cells
• Leukocytic infiltration
• Formation of crescents: Accumulations of proliferating parietal epithelial cells and
infiltrating leukocytes
▪ Basement Membrane Thickening
• Deposition of materials on one side or the other of basement membranes
• Thickening of the basement membrane itself (diabetic glomerulosclerosis)
▪ Hyalinosis and Sclerosis
• Hyalinosis: plasma proteins that have insudated from the circulation into glomerular
structures
◦ **Common feature in focal segmental glomerulosclerosis**
• Sclerosis: accumulations of ECM, either in mesangial areas (diabetics), capillary
loops, or both
• Pathogenesis of Glomerular Injury
◦ Immune Complex Deposition Involving Intrinsic and in Situ Renal Antigens
▪ Anti-GBM Antibody-Induced Glomerulonephritis
• Antibodies directed against normal components of the GBM proper
• **Diffuse linear pattern of staining in immunofluorescent techniques**
• If antibodies cross react with lung BM → Goodpasture syndrome
• The classic antigen responsible is a component of the NC1 domain of α3 chain on
type IV collagen
• **Characterized by severe crescentic glomerular damage and clinical syndrome of
rapidly progressive glomerulonephritis**
◦ Circulating Immune Complex Glomerulonephritis
▪ Trapping of antigen-antibody complexes within glomeruli
• Can be endogenous origin like SLE, or exogenous like streptococci, HbsAg, other
viruses
• **Electron microscopy shows immune complexes as electron-dense deposits that lie
in the mesangium, b/t the outer surface and the GBM (subendothelial deposits), or
b/t the outer surface of the GBM and the podocytes (subepithelial deposits)**
• **Immunofluorescence shows granular deposits along BM, in mesangium, or both*
 ◦ Antibodies to Glomerular Cells
▪ Ab's against glomerular cell antigens may react with cellular components and cause
injury by cytotoxic or other mechanisms
◦ Activation of Alternative Complement Pathway
▪ Happens in dense-deposit disease, aka membranoproliferative glomerulonephritis
(MPGN type II)
◦ Epithelial Cell Injury
▪ Can be seen morphologically as effacement of foot processes, vacuolization, retraction,
and detachment of cells from the GBM
▪ Seen functionally as proteinuria
◦ Mediators of Glomerular Injury
▪ Cells: PMNs, monocytes, macrophages, T cells, NK cells, platelets (release eicosanoids
and growth factors), mesangial cells (can release inflammatory mediators like ROS's,
etc.)
▪ Soluble Mediators: C5b-C9 membrane attack complex, eicosanoids, nitric oxide,
angiotensin, endothelin, cytokines (IL-1 and TNF), chemokines (CCL5, PDGF, TGF-B),
coagulation system
• Mechanisms of Progression in Glomerular Diseases
◦ Focal Segmental Glomerulosclerosis (FSGS)
▪ Adaptive change of healthy glomeruli to diseased kidneys
▪ Adaptive changes (hypertrophy, glomerular HTN, systemic HTN) →
epithelial/endothelial injury → proteinuria
• The adaptive changes also lead to mesangial response that leads to a vicious cycle
◦ Tubulointerstitial Fibrosis
▪ Tubulointerstitial injury (tubular damage and interstitial inflammation) is a component
of many acute and chronic glomerulonephritides
▪ Contributes to progression in both immune and nonimmune diseases
• Nephritic Syndrome
◦ Acute nephritic syndrome may occur in multisystem diseases (SLE and microscopic
polyangiitis)
◦ Usually a characteristic of...
◦ Acute Proliferative (Poststreptococcal, Postinfectious) Glomerulonephritis
▪ 1-4 weeks after strep infection of pharynx or skin, usually kids 6-10
▪ Strep types 12, 4, or 1 in 90% of cases
▪ Cationic antigens (like NAPlr, unique to strep) can be found in affected glomeruli
▪ Morphology:
 • Enlarged, hypercellular glomeruli
• Diffuse proliferation and infiltration of leukocytes (involves all lobules)
• Swelling of endothelial cells → combined w/ everything, obliterates capillary
lumens
• Immunofluorescence shows granular deposits of IgG, IgM, and C3 in mesangium
and along GBM
• EM shows subepithelial “humps”
▪ Clinical:
• Young child abruptly develops malaise, fever, nausea, oliguria, hematuria 1-2 weeks
after recovery from sore throat
• Red cell casts in urine, mild proteinuria, periorbital edema, mild/moderate HTN
◦ Nonstreptococcal Acute Glomerulonephritis (Postinfectious Glomerulonephritis)
▪ Similar to above, but involves different bacteria/virus
• Rapidly Progressive (Crescentic) Glomerulonephritis
◦ RPGN is a syndrome → not associated with a single form of glomerulonephritis
◦ Immunologically mediated
◦ 3 groups:
▪ anti-GBM antibody-induced disease:
• Immunofluorescence shows linear deposits of IgG/C3 in GBM
• In some patients, Ab's cross react with pulmonary alveolar BM's (Goodpasture)
▪ Immune Complex Deposition
• Idiopathic or a complication of postinfectious glomerulonephritis, lupus nephritis,
IgA nephropathy, Henoch-Schonlein purpura
• Immunofluorescence reveals granular pattern (immune complex deposition)
▪ Pauci-immune type
• NO anti-GBM Ab's or immune complexes
• Usually have circulating ANCAs, usually idiopathic
◦ Morphology of all 3:
▪ Severe glomerular injury (**ruptures in GBM**)
▪ Kidneys enlarged, pale, often hemorrhaged on cortex
▪ **Distinctive crescents**
▪ **Fibrin strands are frequently prominent b/t cellular layers in the crescents**
◦ Clinical Findings:
▪ Hematuria, RBC casts, moderate/severe proteinuria, variable HTN and edema
• Nephrotic Syndrome
◦ Many causes; complications can be susceptibility to infections (b/c loss of Ig's) and
 thrombotic/thromboembolic complications (b/c loss of anticoagulants)
◦ Membranous Nephropathy
▪ Idiopathic 85% of the time, otherwise secondary to drugs (penicillamine, captopril, gold,
NSAIDs), underlying malignant tumors, SLE, infections (hep B/C, syphilis, malaria),
other autoimmune disorders
▪ Morphology:
• Uniform, diffuse thickening of the glomerular capillary wall
• Immunofluorescence shows Granular IgG/C3; diffuse
• EM shows subepithelial deposits
▪ Clinical:
• Usually insidious onset of nephrotic syndrome
• Non-selective proteinuria
◦ Minimal-Change Disease
▪ **Most frequent cause of nephrotic syndrome in children, sometimes after infection or
immunization**
▪ **Usually dramatic response to corticosteroid therapy**
▪ Morphology:
• Normal light microscopy
• EM shows diffuse effacement of foot processes of visceral epithelial cells
(podocytes) → replaced by a rim of cytoplasm often showing vacuolization,
swelling, hyperplasia of villi
▪ Clinical:
• Highly selective proteinuria (mostly albumin), normal renal function, no HTN
◦ Focal Segmental Glomerulosclerosis
▪ FSGS occurs in the following settings:
• As a primary disease (idiopathic FSGS)
• In association with HIV, heroin addiction, sickle-cell, massive obesity
• As a secondary event, reflecting scarring of previously active necrotizing lesions,
incases of focal glomerulonephritis (IgA nephropathy)
• Adaptive response to loss of renal tissue in advanced stages of other renal disorders
• Inherited forms of nephrotic syndrome (uncommon)
▪ **Most common cause of adult nephrotic syndrome in US**
▪ Similar to Minimal-change disease, but more hematuria, reduced GFR, HTN,
nonselective proteinuria, poor response to corticosteroids, progression to chronic kidney
disease
▪ Morphology:
 • Light microscopy shows focal and segmental sclerosis and hyalinosis; lipid/foam
cells often present
• Immunofluorescence shows focal IgM/C3
• EM shows loss of foot processes, epithelial denudation
• Collapsing glomerulopathy is a variant of FSGS
▪ Genes involved:
• Genes encoding for nephrin
◦ NPHS1 = Finnish type congenital nephrotic syndrome
◦ NPHS2 mutations = autosomal recessive FSGS and steroid-resistant nephrotic
syndrome in children
◦ Membranoproliferative Glomerulonephritis
▪ Many cases present with a combined nephrotic-nephritic syndrome
▪ Can be primary or secondary
▪ Primary MPGN divided into two types:
• Type I: immune complexes in glomerulus; activation of classic and alternative
complement pathways
• Type II: “dense-deposit disease”; activation of alternative complement pathway (low
C3, normal C1/C4); 70% have antibody called C3 nephritic factor (C3NeF)
▪ Morphology:
• Light microscopy the same in both: glomeruli large and hypercellular, lobular
appearance, GBM is thickened, glomerular cap. wall shows “tram-track” or “double
contour” appearance
• Type I immunofluorescence shows IgG + C3; often C1 + C4; EM shows
subendothelial deposits
• Type 2 immunofluorescence shows IgG + C3; EM shows ribbon like dense deposits
• Isolated Urinary Abnormalities
◦ IgA Nephropathy (Berger Disease)
▪ Frequent cause of recurrent gross or microscopic hematuria
▪ Most common type of glomerulonephritis worldwide
▪ IgA is main Ig in mucosal secretions (seen in celiac disease, lung problems)
▪ Increased IgA1 production → immune complexes trapped in mesangium → activate
alternative complement pathway → glomerular injury
▪ Morphology:
• Light microscopy is variable, but Immunofluorescence shows mesangial deposition
of IgA
• EM shows mesangial and paramesangial dense deposits
 ◦ Hereditary Nephritis (Alport Syndrome and Thin Basement Membrane Lesion)
▪ Alport Syndrome:
• Microscopic hematuria with progression to chronic renal failure, accompanied by
nerve deafness and various eye disorders
• Abnormal COL4A3/COL4A4 (autosomal) or COL4A5 (X-linked)
• EM of GBM shows irregular foci of thickening alternating with thinning, often
producing “basket weave” appearance
• Immunofluorescence shows failure of a3, a4, a5 collagen to stain
▪ Thin Basement Membrane Lesion (Benign Familial Hematuria)
• Asymptomatic hematuria
• Diffuse thinning of GBM
• Chronic Glomerulonephritis
◦ A pool of end-stage glomerular disease fed by several streams of specific types of
glomerulonephritis
◦ Morphology:
▪ Diffusely granular cortical surfaces; cortex is thinned
▪ Increase in peripelvic fat
▪ Eventually, obliteration of glomeruli causing a trap of many proteins, etc.
▪ Arterial and arteriolar sclerosis
▪ Atrophy of associated tubules
▪ Can also exhibit pathology outside the kidneys (uremic complications): uremic
pericarditis/gastroenteritis, secondary hyperparathyroidism, LVH from HTN
• Glomerular Lesions Associated with Systemic Diseases
◦ Lupus Nephritis
◦ Henoch-Schonlein Purpura
▪ Purpuric skin lesions, abdominal pain/vomiting/intestinal bleeding, arthralgia
▪ 1/3 develop renal abnormalities; most common in 3-8 year olds, more severe in adults
▪ IgA nephropathy closely related → similar morphology
◦ Bacterial Endocarditis-Associated Glomerulonephritis
◦ Diabetic Nephropathy
▪ Three glomerular syndromes associated:
• Non-nephrotic proteinuria, nephrotic syndrome, chronic renal failure
▪ Also affects arterioles (hyalinizing arteriolar sclerosis), increases chances of
pyelonephritis, tubular lesions
▪ Morphology shows capillary BM thickening, diffuse mesangial sclerosis, nodular
glomerulosclerosis
 ◦ Amyloidosis
◦ Fibrillary Glomerulonephritis and Immunotactoid Glomerulopathy
▪ Characteristic fibrillar deposits in mesangium and glomerular capillary walls, similar to
amyloidosis but do not stain red and are bigger
▪ Pts develop nephrotic syndrome, hematuria, progressive renal insufficiency; recurs even
after kidney transplants
◦ Other Systemic Disorders
Tubular and Interstitial Diseases
• Diseases that affect tubules usually affect interstitium as well
• 2 major processes: ischemic/toxic tubular injury leading to AKI and acute renal failure, and
inflammatory reactions of the tubules and interstitium (tubulointerstitial nephritis)
• Acute Kidney Injury (AKI) (Acute Tubular Necrosis, ATN)
◦ Acute diminuition of renal function, almost always with evidence of tubular injury
◦ MOST COMMON cause of acute renal failure
◦ 4 common causes:
▪ Ischemia, due to decreased/interrupted blood flow **MOST COMMON**
▪ Direct toxic injury to tubules
▪ Acute tubulointerstitial nephritis (hypersensitivity rxn to drugs)
▪ Urinary obstruction
◦ Reversible
◦ Ischemic ATN
▪ Most often caused by prerenal azotemia due to hypovolemia
▪ Iscliemia damages endothelial cells,
• Causes decrease in vasodilators
◦ Examples—nitric oxide, PCF
• Increase in vasoconstrictors
◦ Example—endothelin
• Net effect is vasoconstriccion of afferent arterioles, which decreases GFR.
▪ Ischemia damages tubular cells
• Causes detachment of tubular cells into the lumen causing obstruction
◦ Produces pigmented renal tubular cell casts → Key Cast in ATN**
▪ Casts obstruct the lumen causing an increase in intratubular pressure.
• Decreases GFR
• Pushes fluid into the interstitium
• Net effect is oliguria.
▪ Sites of tubular damage
 • Straight segment of proximal tubule
◦ • Part of the nephron most susceptible to hypoxia
• Medullary segment ofthe thick ascending limb ('FAD
◦ Location of the Na'-K"-2 Cl cotransporter
• Tubular basement membranes are disrupted at these sites.
◦ Interferes wich renal tubular cell regeneration
◦ Toxic AKI
▪ Aminoglycosides most common cause**, then constrast agents, lead, mercury
▪ Microscopic findings
• Primarily damages the proximal tubule cells
• Tubular basement membrane is intact.
◦ Clinical and laboratory findings in AKI
▪ Oliguria, in most eases
▪ Some cases have polyuria (-800 ml./24 hours).
▪ Pigmented renal tubular cell casts
▪ Hyperkalemia, increased anion gap metabolic acidosis
▪ Increased serum BFN and creatinine (ratio < 15)
▪ Hypokalemia (diuresis phase) and infection are common problems
◦ Treatment
▪ Treat prerenal azotemia
▪ Volume expansion if hypovolemic; increase renal blood llow
▪ Low dose dopamine
▪ Fenoldopam (dopamine a-1-receptor agonist)
▪ Dialysis
• Tubulointerstitial Nephritis
◦ Can be acute or chronic
◦ Causes: acute pyelonephritis (MOST COMMON), drugs, infections, autoimmune, multiple
myeloma, urate nephropathy
◦ Acute Pyelonephritis and UTI
▪ More common in women than men
▪ E. coli most common bacteria (able to adhere well to walls of tract), then Proteus,
Klebsiella, Enterobacter
▪ Polyomavirus is recent common viral cause
▪ Either bacteria get to kidneys from blood (Staph aureus) or ascend up urinary tract
▪ Morphology:
• Hallmarks = patchy interstitial suppurative inflammation, intratubular aggregates of
 neutrophils, and tubular necrosis. Also, pyelonephritic scar forms in healing phase**
▪ Clinically:
• Sudden onset, pain @ costovertebral angle, fever/malaise,
dysuria/frequency/urgency
• Pyuria, leukocyte casts in urine → high in neutrophils (pus casts) = renal
involvement
• Complications = papillary necrosis, pyonephrosis, perinephric abscess, chronic PN
◦ Chronic Pyelonephritis (CPN) and Reflux Nephropathy
▪ Chronic tubulointerstitial inflammation and renal scarring are associated with pathologic
involvement of the calyces and pelvis
▪ Reflux type of CPN
• U-shaped cortical scars overlying a blunt calyx
• Visible with an intravenous pyelogram (IVP)
▪ Obstructive type CPN
• Uniform dilation of the calyces
• Diffuse thinning of cortical tissue
▪ Microscopic findings
• Chronic inflammation
◦ Secondary scarring of the glomeruli
• Tubular atrophy
◦ Tubules contain eosinophilic material resembling thyroid tissue
(“thyroidization”)
▪ Clinical and laboratory findings
• Usually a history of recurrent APN
• May cause hypertension
◦ Reflux nephropathy is a cause of hypertension in children,
▪ May cause chronic renal failure (CRF)
◦ Acute Drug-Induced Interstitial Nephritis
▪ Synthetic penicillins (amp, meth), rifampin, sulfonamides, thiazide diuretics, NSAIDS
▪ Combination of Type I and IV hypersensitivity
▪ Occurs 2 weeks after beginning a drug
▪ Eosinophils and neutrophils may be present; giant cells, “tubulitis”
◦ Analgesic Nephropathy
▪ Common in women, common in pts with chronic pain
▪ **Papillary necrosis develops first, then cortical tubulointerstitial nephritis follows
◦ Urate Nephropathy
 ▪ Deposition of urate crystals in the tubules antl interstitium
▪ Causes
• Massive release of purines (precursor of uric acid)
◦ usually following aggressive treatment of disseminated cancer (e.g., leukemia)
• Lead poisoning, gout
▪ May produce ARF
◦ Hypercalcemia and Nephrocalcinosis
▪ Deposition of calcium in the kidney secondary to hypercalcemia
▪ Alternating areas of normal and scarred parenchyma (from atrophy of entire cortical
areas drained by calcified tubules
▪ Inability to concentrate urine
◦ Acute Phosphate Nephropathy
▪ Pt consumes high doses of oral phosphate sol'ns for colonoscopy → accumulations of
calcium phosphate crystals in tubules
▪ Pt's only partially recover from renal damage
◦ Light-Chain Cast Nephropathy(“Myeloma Kidney”)
▪ Overt renal insufficiency in 50% of pt's with multiple myeloma
▪ Mechanisms:
• Bence Jones (BJ) proteinuria
◦ BJ protein produces tubular casts.
▪ Light chains arc coxic co renal tubular epithelium.
◦ Casts obstruct the lumen and incite a foreign body giant cell reaction.
▪ Reaction involves tubules and interstitium leading to renal failure,
• Nephrocalcinosis
◦ Due to hypercalcemia
▪ Metastatic calcification of the basement membrane of collecting tubules
◦ Causes polyuria and renal failure
• Primary amyloidosis producing nephrotic syndrome
◦ Light chains are converted to amyloid
▪ Morphology:
• BJ tubular casts = pink to blue amorphous masses, fill/distend tubular lumens
• Some casts are surrounded by multinucleate giant cells
Vascular Diseases
• Benign nephrosclerosis (BNS)
◦ Most common renal disease in essential hypertension
◦ Pathogenesis
 ▪ Hyaline arteriolosclerosis of arterioles in the renal cortex,
▪ Causes tubular atrophy, interstitial fibrosis, glomerular sclerosis
◦ Small kidneys with a finely granular cortical surface
◦ Laboratory fintlings
▪ Mild proteinuria
▪ Hematuria (no RBC casts)
▪ Renal azotemia
• Malignant Hypertension and Accelerated Nephrosclerosis
◦ Sudden onset of aceelerated hypercension
▪ May occur in normotensive individuals
▪ May occur in those with BNS (most common)
▪ May occur as a complication of various disorders
◦ Risk factors
▪ Pre-existing BNS (most common)
▪ Hemolytic-uremic syndrome
▪ Thrombotic thrombocytopenic purpura
▪ Systemic sclerosis
◦ Pathogenesis
▪ Vascular damage to arterioles and small arteries
▪ Gross and microscopic changes:
• Fibrinoid necrosis and necrotizing arteriolitis and glomerulitis
◦ Pinpoint hemorrhages on the cortical surface ("flea-bitten" kidneys)
• Hyperplastic arteriolosclerosis ("onion skin" lesion)
◦ Smooth muscle hyperplasia and reduplication of basement membrane
◦ Clinical findings
▪ Rapid increase in blood pressure to >210/l20
▪ Hypertensive encephalopathy
• Cerebral edema
• Papilledema
• Retinopathy
◦ Flame hemorrhages, exudates
• Potential for an intracerebral bleed
▪ Oliguric acute renal failure
◦ Laboratory findings
▪ Azotemia with BUN:Cr ratios < 13
▪ Hematuria wich RBC eases
 ▪ Proteinuria
◦ Initial treatment is intravenous sodium nitroprusside.
• Renal Artery Stenosis
◦ Uncommon cause of HTN, but is potentially curable with surgical treatment
◦ Constriction of one renal artery results in HTN
◦ Most common cause is occlusion by artheromatous plaque at the origin of the renal artery
(70% of cases, more in men)
◦ Another cause is fibromuscular dysplasia → fibrous/fibromuscular thickening, usually the
medial adventitia, more common in women, 30s and 40s
• Thrombotic Microangiopathies
◦ Typical HUS:
▪ Usually after E. coli infection or Shigella infection
▪ Severe oliguria, hematuria, hemolytic anemia, thrombocytopenia
◦ Atypical HUS:
▪ Inherited mutations of complement regulatory proteins (usually factor H)
▪ Acquired causes: antiphospholipid antibodies, complications of pregnancy or birth
control, HTN, scleroderma, chemo/radiation
◦ TTP:
▪ Inherited or acquired deficiencies of ADAMTS13 (regulates function of vWF)
▪ CNS involvement is the dominant feature, renal involvement in 50%
◦ All of these show similar morphologies;
▪ If acute:
• Platelets aggregate and occlude glomerular capillaries
• Capillary walls thickened, endothelial swelling, subendothelial deposits
▪ If chronic (Atypical HUS and TTP ONLY)
• Scarring or renal cortex
• Double contours or tram tracks (reduplication of BM)
• Onion skinning in arteries and arterioles
• Other Vascular Disorders
◦ Renal Infarcts
▪ Causes
• Embolization from thrombi in the left side of the heart (most common)
• Artheroembolic renal disease
• Vasculitis, particularly polyarteritis nodosa
▪ Gross and microscopic appearance
• Irregular, wcdgc-shapcd pale infarctions in the cortex
 • Old infarcts have a V-shaped appearance due to scar tissue
▪ Sudden onset of flank pain antl hemacuria
◦ Sickle cell Nephropathy
▪ Clinical presentations
• Asymptomatic hematuria (most common)
◦ Due to infarctions in the medulla
• Loss of concentrating ability
• Renal papillary necrosis
• Pyelonephritis
◦ Diffuse cortical necrosis
▪ Complication of an obstetric emergency
• Examples—preeclampsia, abruptio placentae
▪ Due to DIC; limited to the renal cortex
• Fibrin clots in arterioles and glomerular capillaries
• Bilateral, diffuse, pale infarct of the renal cortex
◦ Anuria (no urine) in a pregnant woman followed by ARF