Renal Pathology

Nephrotic

Nephritic

profound proteinuria

no evidence of cellular inflammatory response

immune complex deposition at or under epithelial cells

morphologic changes in foot process

damage to selectivity filter

red/white cells in urine

Immune complex deposition in sub endothelial or glomerular basement membrane or mesangium

inflammatory reaction

severe edema

hyperlipidemia/lipiduria

results from glomerular injury

edema

hypertension

Acute kidney disease

oliguria/anuria

recent onset of azotemia

results from glomerular injury, interstitial injury, vascular injury or tubular injury

rapid deterioration of function that accumulates nitrogenous wastes

Chronic Kidney Disease

buildup of nitrogen products, hormones, and EPO

results from progressive scarring in kidney

requires dialysis or transplantation

UTI

bateriuria and pyuria

symptomatic/asymptomatic

may only affect kidney or bladder

Nephrolithiasis

renal stones

renal colic calculus formation caused by increased urinary concentration

hematuria (without red cell casts)

Glomerular Diseases

can originate in the kidney

combination of hematuria, proteinuria, reduced GFR, and hypertension

oliguria/azotemia

Acute GN

Acute Glomerulonephritis

abrupt onset of hematuria and proteinuria with reduced GFR and renal salt and water retention

infectious disease

tissue injury caused by complement activation by classical pathway

Rapidly Progressive glomerulonephritis

at least 50% glomerular filtration failure

"crescentic GN" -- cellular crescents in bowman space formed in response to severe damage to glomerular capillaries limited to kidney

antiglomerular basement membrane antibody disease

caused by development of circulating antibodies to an antigen intrinsic to glomerular basement membrane

binding of pathologic anti-GBM antibodies to glomerular basement membrane causes inflammation

Anti-neutrophil cytoplasmic antibody (ANCA)

lack of anti-GBM antibodies or of significant immune complex deposition
may be renal or systemic

found in serum

crescentic GN

linear deposits of IgG

Immune complex glomerulonephritis

granular immunoglobulin deposits suggestive of immune complexes from systemic disease

Ex. post infectious GN where there is cross reactivity between antigen of infecting organism and host antigen and results in deposition of immune complexes and complement in glomerular capillaries

Chronic Glomerulonephritis

persistent urinary abnormalities, slowly progressive decline in renal function

does not resolve

Cellular Proliferation in either mesangium or capillary

obliteration of glomeruli

Asymptomatic urinary abnormalities

hematuria and proteinuria with no functional abnormalities

causes: IgA nephropathy or thin basement membrane

Immune complex disease with mesangial IgA deposition

Minimal Change Disease

hypoalbuminemia

benign

most frequent cause of nephrotic syndrome in children

normal glomerular basement membrane, diffuse effacement of podocytes

Focal segmental glomerulosclerosis (FSGS)

sclerosis of some glomeruli

Primary caused by injury to podocytes [could also be secondary to other conditions]

Membranous Nephropathy

subepithelial immunoglobulin deposits along GBM

well developed cases have diffuse thickening of glomerular capillary wall

usually caused by autoantibodies that cross react with antigens expressed by podocytes

working hypothesis: complement activation leads to C5-9 MAC which damages mesangial cells and podocytes directly --> loss of slit filter integrity and proteinuria

Tubules/ Interstitium Nephritis

inflammatory diseases

glomeruli may be unaffected

usually caused by bacterial infection

pyelonephritis [renal pelvis prominently involved]

caused by bacterial infection like UTI and enteric gram negative rods

Usually Ascending infection via blood stream

Discrete, yellowish, raised abscesses on renal surface

Acute Tubular Injury

granular casts/tubular cells in urine

decreased GFR

electrolyte abnormalities, acidosis, uremia, fluid overload but oliguria

results from ischemic or toxic injury to renal tubules

infrarenal vasoconstriction so diminished delivery of O2 and nutrients to tubular cells

Na/water excess,

hyperkalemia if reduced GFR below 5mL/min, otherwise aldosterone-mediated K transport in distal tubule increases

decreased renin production --> decreased angiotensin II --> impaired aldosterone secretion --> can't excrete K

Results in: diminished Ca absorption, overproduction of parathyroid hormone, disordered vitamin D metabolism, phosphorous retention, chronic metabolic acidosis

Hematologic abnormalities: normocytic anemia, increased bruising, decreased clotting, infection susceptibility

GI abnormalities: anorexia, hiccups, nausea, vomiting

endocrine and metabolic abnormalities: low estrogen levels, low testosterone, half life of insulin increases

calcium oxalate/calcium phosphate ---- magnesium ammonium phosphate---- uric acid/cystine stones

pain caused by distention

complications: 1) hydronephrosis 2) infection 3) renal damage 4) hypertension from increased renin production

Cystic Diseases

Adult polycystic kidney disease

multiple expanding cysts on both kidneys that destroy parenchyma

10% of chronic kidney disease

PKD1 on short arm of chromosome-- polycystic-1

Kidney Tumors

renal cell carcinoma

clear cell carcinomas (clear cytoplasm)

von Hippel-Lindau disease