Renal Pathology

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Simple Renal Cyst

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Translucent, lined with gray, glistening, smooth membrane with clear fluid

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Multicystic Renal Cyst

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Presence of islands of undifferentiated mesenchyme often with cartilage and immature collecting ducts

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Autosomal Recessive Polycystic Disease

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PKHD1 gene mutation

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Autosomal Recessive Polyscystic Disease

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Enlarge kidneys with smooth external appearance

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Autosomal Dominant Polycystic Disease

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Multiple expanding cysts and ultimately destroys renal parenchyma

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Autosomal Dominant Polycystic Disease

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PKD1 and PKD2 gene mutation

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Autosomal Dominant Polycystic Kidney Disease

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External surface composed of mass of cysts with no intervening parenchyma

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Autosomal Dominant Polycystic Disease

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Insidious onset of hematuria followed with proteinuria, polyuria and hypertension

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Acquired (Dialysis-Associated) Cystic Disease

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Patient with end-stage renal disease who undergone prolonged dialysis

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Acquired Cystic Disease

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12- to 18-fold increased risk of renal cell carcinoma

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Medullary Sponge Kidney

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Multiple cystic dilations of the collecting ducts in the medulla

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Nephronopthisis

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Usually concentrated at corticomedullary junction and cortical tubulointerstitial damage causes renal insufficiency

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Adult-Onset Medullary Cystic Disease

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Autosomal dominant mutation of MCKD1 and MCKD2

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Primary Glomerulonephritis

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Disorders in which kidney is the only or predominant organ involved

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Secondary Glomerulonephritis

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Systemic immunologic disease often affect the glomerulus

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Glomerulopathy

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Do not have cellular inflammatory component

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Hypercellularity

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Proliferation of mesangial and endothelial cells, infiltration of leukocytes including neutrophils, monocytes, and lymphocytes, and formation of crescents

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Basement Membrane Thickening

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Deposition of amorphous electron-dense material on the endothelial or epithelial side of BM

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Basement Membrane Thickening

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Increased synthesis of the protein components of the basement membrane

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Basement Membrane Thickening

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Formation of additional layers of basement membrane matrices

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Hyalinosis

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Accumulation of material that is homogenous and eosinophilic

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Sclerosis

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Deposition of extracellular collagenous matrix

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Diffuse

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Involving all of the glomeruli in the kidney

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Global

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Involving the entirety of individual glomeruli

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Focal

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Involvong only a fraction of the glomeruli in the kidney

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Segmental

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Affecting a part of each glomerulus

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Nephritic Syndrome

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Inflammation in the glomeruli with hematuria, red cell casts, azotemia, oliguria, and mild to moderate hypertension

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Acute Proliferative Glomerulonephritis

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Diffuse proliferation of glomerular cells associated with influx of leukocytes

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Poststreptococcal Glomerulonephritis

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Appears 1 to 4 weeks after streptococcal infection of the pharynx or skin

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Poststreptococcal Glomerulonephritis

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Enlarged hypercellular glomeruli caused by infiltration by neutrophils and monocytes, proliferation of mesangial and endothelial cells and with crescent formation

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Rapidly Progressive Glomerulonephritis

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Rapid and progressivr loss of renal function associated with severe oliguria

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Rapidly Progressive Glomerulonephritis

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Most common histologuc picture is presence of crescents in most of the glomeruli

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Rapidly Progressive Glomerulonephritis

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Proliferation of the parietal epithelial cells lining Bowman capsule and infiltration of monocytes and macrophages

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Type I (Anti-GBM Antibody) RPGN

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Linear deposits of IgG and C3 in the GBM

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Type I (Anti-GBM Antibody) RPGN

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Renal limited or associated with Goodpasture Syndrome

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Type II (Immune Complex) RPGN

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Complication of any immune complex nephritides

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Type III (Pauci-Immune) RPGN

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Lack of detectable anti-GBM antibodies or immune complexes

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Type III (Pauci-Immune) RPGN

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With antineutrophil cytoplasmic antibodies

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Nephrotic Syndrome

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Massive protenuria (3.5 gm), hypoalbuminemia (<3 gm/dL), geberalized edema, hyperlipidemia and lipiduria

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Nephrotic Syndrome

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Thrombotic and thromboembolic complications, renal vein thrombosis, vulnerable to infections

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Membranous Nephropathy

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Diffuse thickening of the glomerular capillary wall due to accumulation of deposits containing Ig along subepithelial side of basement membrane

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Membranous Nephropathy

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Associated with drugs, underlying malignant tumors, SLE, infections and other autoimmune disorders

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Membranous Nephropathy

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Indisious onset of nephrotic syndrome with hematuria and mild hypertension

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Minimal Change Disease

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Most common cause of nephrotic syndrome in children

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Minimal Change Disease

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Effacement of foot processes of visceral epithelial cells detectable only by electron microscopy

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Minimal Change Disease

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Dramatic response to corticosteriod therapy

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Focal Segmental Glomerulosclerosis

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Most common cause of nephrotic syndrome in adults

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Focal Segmental Glomerulosclerosis

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Can be a primary disease, in association with HIV, heroin addiction, sickle cell disease, and massive obesity

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Focal Segmental Glomerulosclerosis

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As a secondary event, with scarring of inactive necrotizing lesions, component of adaptive response to loss of renal tissue and uncommon inherited mutations of proteins localized to slit diaphragm

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Collqpsing Glomerulopathy

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Morphologic variant of FSGS characterized by retraction and collapse of entire glomerular tuft

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Membranoproliferative Glomerulonephritis

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Alterations in the glomerular basement membrane, proliferation of glomerular cells, leukocyte infiltration, and presence of deposits in mesangial region and glomerular capillary walls

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Type I Primary MPGN

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Evidence of immune complexes in the glomerulus and activation of both classical and alternative complement pathways

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Type I Primary MPGN

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IgG and C3 are deposited in a granular pattern, and early complement components (C1q and C4) are present

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Type II Primary MPGN

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Dense deposit disease

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Type II Primary MPGN

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Abnormalities resulting in excessive activation of the alternative complement pathway

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Secondary MPGN

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Associated with chronic immune complex disorders, alpha-1 antritrypsin deficiency and malignant disease

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IgA Nephropathy

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Berger Disease

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IgA Nephropathy

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Presence of prominent IgA deposits in the mesangial regions and recurrent hematuria

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IgA Nephropathy

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Most common type of glomerulonephritis worldwide

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Alport Syndrome

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Manifest by hematuria with progression to chronic renal failure accompanied by nerve deafness and various eye disorders

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Alport Syndrome

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X-linked trait commonly with hematuria accompanied by renal cell cast

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Thin Basement Membrane Lesion

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Familial asymptomatic hematuria and morphologically by diffuse thinning of GBM

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Chronic Glomerulonephritis

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Kidneys symmetrically contracted and diffusely granular cortical surfaces

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Chronic Glomerulonephritis

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Cortex is thinned with increase in peripelvic fat and obliteration of glomeruli

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Chronic Glomerulonephritis

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Accompanied with hypertension and arterial and arteriolar sclerosis

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Chronic Glomerulonephritis

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Marked atrophy of associated tubules, irregular interstitial fibrosis, and mononuclear leukocytic infiltration

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Lupus Nephritis

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Recurrent miccroscopic or gross hematuria, nephritic syndrome, type II RPGN, nephrotic syndrome, acute and chronic renal failure and hypertension

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Henoch Schonlein Purpura

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Purpuric lesions, abdominal pain and intestinal bleeding and arthralgias

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Henoch Schonlein Purpura

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Gross or microscopic hematuria, nephritic syndrome, nephrotic syndrome, or some combination and develop rapidly progressive glomerulonephritis with many crescent

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Diabetic Nephropathy

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Capillary basement membrane thickening, diffuse mesangial sclerosis, nodular glomerulosclerosis, Kimmelsteil-Wilson lesion

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Acute Tubular Injury

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Acute renal failure, morphologic evidence of tubular tubular injury in the form of necrosis of tubular epithelial cells

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Acute Tubular Necrosis

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Most common cause of acute kidney injury

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Acute Tubular Injury

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Manifests with oliguria (<400 mL)

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Ischemic Acute Tubular Injury

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Necrosis is patchy, relatively short length of tubules are affected

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Ischemic Acute Tubular Injury

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Straight segment of proximal tubules and ascending limbs of Henle's loop are most vulnerable

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Ischemic Acute Tubular Injury

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There is rupture of the basement membrane

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Toxic/Nephrotoxic Acute Tubular Injury

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Extensive necrosis along the proximal convuluted tubule segmentswith many toxins

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Toxic/Nephrotoxic Acute Tubular Injury

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Basement membrane is spared

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Acute Tubular Injury

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Lumens of DCT and collectinf ducts contain eosinophilic hyaline casts as well as pigmented granular casts

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Acute Tubular Injury

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Tamm-Horsfall protein

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Initiation Phase

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Lasting about 36 hours indicatedwith decline in urine output with rise in BUN

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Maintenance Phase

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2nd to 6th day with sustained decrease in urine output (40 and 400 mL/day), salt and water overload, rising BUN, hyperkalemia, metabolic acidosis and uremia

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Recovery Phase

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Steady increase in urine volume (3L/day) with hypokalemia

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Tubointerstitial Nephritis

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Inflammatory injuries of the tubules and interstitium that are insidious in onset and azotemia

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Acute Tubulointerstitial Nephritis

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Rapid clinical onset with interstitial edema, leukocytic infiltration and tubular injury

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Chronic Interstitial Nephritis

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Infiltration with mononuclear leukocytes, interstitial fibrosis and wide-spread tubular atrophy

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Ascending Infection

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Most common cause of clinical pyelonephritis

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Pyelonephritis

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Inflammation affecting the tubules, interstitium, and renal pelvis

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Acute Pyelonephritis

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Suppurative inflammation of the kidney caused by bacterial and viral infection

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Acute Pyelonephritis

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Patchy suppurative inflammation, intratubular aggregates of neutrophils, neutrophilic tubulitis and tubular necrosis

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Chronic Pyelonephritis

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Chronic tubulointerstitial inflammation and scarring involving calyces and pelvis

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Chronic Pyelonephritis

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Coarse, discrete, corticomedullary scars overlying dilated, blunted, or deformed calyces, snd flattening of the papillae

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Chronic Pyelonephritis

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Dilqted tubules with fĺattened epithlium may be filled with castsresembling thyroid colloid

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Xanthogranulomatous Pyelonephritis

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Accumulation of foamy macrophages intermingled with the plasma cells, lymphocytes, polymorphonuclear leukocytes and giant cells

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Xanthogranulomatous Pyelonephritis

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Produce large, yellowish orange nodules grosslt confused with renal cell carcinoma

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Tubulointerstitial Nephritis Induced by Drugs and Toxins

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Second most common cause of acute kidney injury

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Tubulointerstitial Nephritis Induced by Drugs and Toxins

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Trigger an interstitial immunologic reaction

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Aristocholic Nephropathy

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Supplement in herbal remedies

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Aristocholic Nephropathy

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Forms covalent adducts with DNA

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Aritocholic Nephropathy

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Balkan endemic nephropathy

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Acute Uric Acid Nephropathy

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Caused by precipitation of uric acid crystals in renal tubules leading to obstruction

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Chronic urate nephropathy

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Monosodium urate crystals deposite in the acidic millieu of DCT and CT

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Chronic Urate Nephropathy

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Form birefringement needle-like crystals

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Nephrolithiasis

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Uric acid stones present with gout of those secondary hyperuricemia

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Nephrocalcinosis

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Formation of calcium stones and deposition of calcium

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Benign Nephrosclerosis

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Moderate reduction in renal plasma flow, moderate proteinuria, GFR is normal

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Benign Nephrosclerosis

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Medial and intimal thickening, hyalinization of arteriolar walls and increased deposition of basement membrane matrix

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Benign Nephrosclerosis

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Cirtical surfaces have fine, even granularity that resembles grain leather

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Benign Nephrosclerosis

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Narrowing of lumens of arteriolar and small arteries, patchy ischemic atrophy with tubular atropht and interstitial fibrosis and glomerular alterations

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Malignant Nephrosclerosis

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Markedly elevated levels of plasma renin

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Malignant Nephrosclerosis

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Small, pinpoint petechial hemorrhages on cortical surface giving "fleabitten" appearance

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Malignant Nephrosclerosis

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Fibrinoid necrosis, necrotizing arteriolitis, hyperplastic arteriosclerosis (onion-skinning), necrotizing glomerulitis

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Malignant Nephrosclerosis

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Systolic pressure greater than 200 mmHg and diastolic pressure greater thwn 120 mmHg

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Malignant Nephrosclerosis

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Papilledema, retinal hemorrhages, encephalopathy, cardiovascular abnormalities and renal failure

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Renal Artery Stenosis

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Caused by narrowing at the origin by atheromatous plaque and fibromuscular dysplasia

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Hydronephrosis

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Dilation of renal pelvis and calyces associated with progressive atrophy of the kidney due to obstruction to outflow of urine

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Typical Hemolytic Uremic Syndrome

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Epidemic, classic, diarrhea-positive associated wih consumption of food contaminated by bacteria producing Shiga-like toxin

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Atypical Hemolytic Uremic Syndrome

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Non-epidemic, diarrhea-positive associated inherited mutations of complement-regulatory proteins

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Thrombotic Microangiopathies

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Hemolytic anemia, thrombocytopenia, renal failure, and tnrmbotic lesions in capillaries and arterioles

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Calcium Stones

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Hyperabsorption of calcium, intrinsic impairment in renal tubule reabsorption of calcium

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Triple/Struvite Stones

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Formed after infections by urea-splitting bacteria

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Struvite Stones

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Largest stones so called staghorn calculi

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Uric Acid Stones

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Common in hyperuricemia with gout

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Renal Papillary Adenoma

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Small, discrete adenomas arising from the renal tubular epithelium grossly pale yellow-gray, discrete, well circumscribed nodules with complex branching, papillomatous structures

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Angiomyolipoma

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Benign neoplasm consisting of vessels, smooth muscles, and fat from perivascular epithelioid cells

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Angiomyolipoma

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With tuberous sclerosis, a disease caused by loss of function mutation in TSC1 or TSC2

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Oncocytoma

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Epithelial neoplasm composed of large eosinophilic cells having small, round, benign-appearing nuclei that have large nuclei

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Clear Cell Carcinoma

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Most common renal cell carcinoma composed of clear or granular cytoplasm and are nonpapillary

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Chromophobe Carcinoma

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With prominent cell membranes and pale eosinophilic cytoplasm, usually with halo

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Collecting Duct (Bellini duct) Carcinoma

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Renal carcinoma arising from collecting duct cells in he medulla

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Renal Cell Carcinoma

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Costovertebral pain, palpable mass, hematuria

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Urothelial Carcinoma

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Produce noticeable hematuria and painless

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Autosomal Dominant Polycystic Kidney Disease

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External surface composed of mass of cysts with no intervening parenchyma

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Autosomal Dominant Polycystic Kidney Disease

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Cysts filled with clear, serous fluid or with turbid red brown hemorrhagic fluid

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Acquired (Dialysis-Associated) Cystic Disease

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12- to 18-fold increased risk of renal cell carcinoma