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