kidney

RENAL PATHOLOGY

NORMALCONGENITAL“CYSTS”GLOMERULARTUBULAR/INTERSTITIALBLOOD VESSELSOBSTRUCTIONTUMORS


1. Renal Vein2. Renal Artery3. Renal Calyx4. Medullary Pyramid5. Renal Cortex6. Segmental Artery7. InterlobAR Artery8. Arcuate Artery interlobULAR9. Arcuate Vein10. Interlobar Vein11. Segmental Vein12. Renal Column13. Renal Papillae14. Renal Pelvis15. Ureter

S.E.M.

T.E.M.

CONGENITAL

AGENESIS HYPOPLASIA ECTOPIC HORSESHOE

AGENESIS

HYPOPLASIA

ECTOPIC (usually PELVIC)

HORSESHOE

CYSTIC DISEASES

CYSTIC RENAL “DYSPLASIA”Autosomal DOMINANT (AD-ULTS)Autosomal RECESSIVE (CHILDREN)MEDULLARYMedullary Sponge Kidney (MSK)Nephronopththisis-MedullaryACQUIREDSIMPLE

CYSTIC RENAL “DYSPLASIA” ENLARGEDUNILATERAL or BILATERALCYSTICHave “MESENCHYME”NEWBORNSVIRAL, GENETIC (rare)

AUTOSOMAL DOMINANT

HEREDITARY, PKD1, PKD2FOLLOWS AUTOSOMAL DOMINANT PEDIGREECOMPLEX GENETICSRENAL FAILURE in 50’s

AUTOSOMAL RECESSIVE

CHILDHOOD KIDNEYS LOOK EXACTLY LIKE THE ADULT TYPE PKHD1 PATIENTS WHO SURVIVE CHILDHOOD OFTEN DEVELOP HEPATIC FIBROSIS

ACQUIRED (DIALYSIS)

“SIMPLE” CYSTS CorticalAlso called “retention” cystsAlso “acquired”Incidental, asymptomaticVERY very very common

GLOMERULAR DISEASESaka, glomerulonephropathies

PATHOLOGIC MANIFESTATIONS
CELLULAR PROLIFERATION Mesangial Endothelial LEUKOCYTE INFILTRATION CRESCENTS (RAPIDLY progressive) BASEMENT MEMBRANE THICKENING HYALINIZATION SCLEROSIS

PATHOGENESIS

Antibodies against inherent GBMAntibodies against “planted” antigensTrapping of Ag-Ab complexesAntibodies against glomerular cells, e.g., mesangial cells, podocytes, etc.Cell mediated immunity, i.e., sensitized T-cells as in TB

ACUTE GLOMERULONEPHRITIS

Hematuria, Azotemia, Oliguria, in children following a strep infection POSTSTREPTOCOCCAL (old term) HYPERCELLULAR GLOMERULI INCREASED ENDOTHELIUM AND MESANGIUM IgG, IgM, (not IgA), C3 along GMB FOCALLY 95% full recovery


“RAPIDLY PROGRESSIVE” GLOMERULONEPHRITIS Clinical definition, NOT a specific pathologic one“CRESCENTIC”Anti-GBM AbIMMUN CPLXAnti-Neut. Ab


NEPHROTIC SYNDROME
MASSIVE PROTEINURIA HYPOALBUMINEMIA EDEMA LIPIDEMIA/LIPIDURIA NUMEROUS CAUSES: MEMBRANOUS, MINIMAL CHANGE, FOCAL SEGMTL. DIABETES, AMYLOID, SLE, DRUGS

MEMBRANOUS GLOMERULONEPHRITIS

Drugs, Tumors, SLE, Infections Deposition of Ag-Ab complexes Indolent, but >60% persistent proteinuria 15% go on to nephrotic syndrome

MINIMAL CHANGE GLOM.(LIPOID NEPHROSIS)

MOST COMMON CAUSE of NEPHROTIC SYNDROME in CHILDREN EFFACEMENT of FOOT PROCESSES

FOCAL SEGMENTAL GLOMERULO-SCLEROSIS

Just like its nameFocalSegmentalGlomerulo-SCLEROSIS (NOT –itis)HIV, Heroine, Sickle Cell, ObesityMost common cause of ADULT nephrotic syndrome

TUBULESINTERSTITIUMBLOOD VESSELSOBSTRUCTIONTUMORS

TUBULAR DISEASES
ACUTE TUBULAR NECROSIS TUBULOINTERSTITIAL NEPHRITIS PYELONEPHRITIS ACUTE CHRONIC DRUGS TOXINS URATE NEPHROPATHY HYPERCALCEMIA/NEPHROCALCINOSIS MULTIPLE MYELOMA

ACUTE TUBULAR NECROSIS

Destruction of renal TUBULAR epithelium Loss of renal function 50% of ACUTE renal failure Two types: ISCHEMIC NEPHROTOXIC -AMINOGLYCOSIDES -AMPHOTERICIN B -CONTRAST AGENTS

NORMAL

ATN

ATN PATHOGENESIS

BLOOD FLOW DISTURBANCES (ISCHEMIC) TUBULAR INJURY (NEPHROTOXIC)

PYELONEPHRITIS

GI Gram NEGATIVES: E. COLI, Proteus, Klebsiella, Enterobacter, Strep. faecalis, usually “NORMAL” floraASCENDING, by FAR, the most common, i.e., reflux, obstructionHEMATOGENOUS tooACUTE PYELONEPHRITIS, neutrophilsCHRONIC PYELONEPHRITIS, lymphocytes, scars

ACUTE or CHRONIC PYELONEPHRITIS?

ACUTE or CHRONIC PYELONEPHRITIS?

ACUTE or CHRONIC PYELONEPHRITIS?

FACTORS
OBSTRUCTION: Congenital or Acquired INSTRUMENTATION VESICOURETERAL REFLUX PREGNANCY AGE, SEX, why sex? F>>>M PREVIOUS LESIONS IMMUNOSUPPRESION or IMMUNODEFICIENCY

NORMAL

VASCULAR DISEASES
BENIGN NEPHROSCLEROSIS MALIGNANT NEPHROSCLEROSIS (i.e., malignant hypertension) RENAL ARTERY STENOSIS THROMBOTIC MICROANGIOPATHIES Hemolytic-Uremic Syndromes, Child, Adult, TTP THROMBI, EMBOLI, INFARCTS SICKLE CELL DIFFUSE CORTICAL NECROSIS

BENIGN NEPHROSCLEROSIS

Sclerosis, i.e., “hyalinization” of arterioles and small arteries, i.e., arterio-, arteriolo-Is this part of “routine” atherosclerosis????VERY VERY VERY common

MALIGNANT NEPHROSCLEROSIS (i.e., malignant hypertension)

NOT a part of “routine” atherosclerosisBy definition, associated with rapidly progressive hypertension (1-2% of HTN)VASCULAR DAMAGEFIBRINOID NECROSIS“ONION SKINNING”SIGNIFICANT LUMENAL NARROWING

What is “onion-skinning”?What is an onion?What is “fibrinoid” necrosis?

RENAL INFARCTS
WEDGE SHAPED WELL DELINEATED“WHITE” (anemic) INFARCTPerhaps a little “YELLOW”HEAL WITH A SCAR

OBSTRUCTIONS

UROLITHIASIS CONGENITAL PROSTATE ENLARGEMENT TUMORS INFLAMMATION SLOUGHED CLOTS, PAPILLAE PREGNANCY NEUROGENIC

UROLITHIASIS

CALCIUM (OXALATE or PHOSPHATE) 70% MAGNESIUM AMMONIUM PHOSPHATE 20% URIC ACID 10%
CA↑↑↑Bact.U.A. ↑↑↑

TUMORS

BENIGN Papillary Adenoma (SIZE very important) Fibroma/Hamartoma Angiomyolipoma Oncocytoma (very red, granular, mitochondria) MALIGNANT Renal Cell Carcinoma (Clear Cell Carcinoma, Adenocarcinoma, Hypernephroma) Urothelial (Transitional)

RENAL CELL CARCINOMA

TOBACCO RELATED, STRONGLYSOME HEREDITARY/FAMILIALMOST are “CLEAR CELL”, a few PAPILLARYYELLOW grossly, “CLEAR” cells microscopicallySTRONGLY tend to invade the renal VEIN early, in preference to lymphatics. Does the kidney have lymphatics?