Causes of Nephrotic Syndrome in Adults and Glomerular Lesions

Renal colic, hematuria, and recurrent stone formation.

Glomerular, Tubular, Interstitial, Vascular.

Endogenous (as in SLE) or Exogenous (bacterial, viral, parasitic, spirochetal infections) or Unknown.

Activation of the complement system.

Anti-GBM antibody GN.

Antibodies to visceral epithelial cell antigens.

Progression to end-stage renal failure.

Massive proteinuria, hypoalbuminemia, generalized edema, hyperlipidemia, and lipiduria.

Minimal-Change Disease (MCD)

Focal and Segmental Glomerulosclerosis (FSGS)

Selective proteinuria

IgA nephropathy

GBM thickening and proliferation of glomerular cells

Diabetes, Amyloidosis, SLE

Caused by circulating immune complexes

Hematuria, Oliguria with azotemia, Hypertension

Deposition of IgA in the mesangium

1. Rapidly progressive loss of renal function. 2. Nephritic syndrome. 3. Severe oliguria. 4. Death from renal failure within weeks to months if untreated

Discrete, yellowish, raised abscesses on the renal surface

Through the bloodstream or from the lower urinary tract (ascending infection)

Properties of both the urothelium and the offending bacteria

Bacterial adhesion to the urethral urothelium and gaining access to the bladder

Due to factors facilitating entry of bacteria to the bladder such as short urethra and close proximity of the urethra to the rectum

Incomplete bladder emptying and increased residual volume of urine

Elevation of blood urea nitrogen and creatinine levels

1. Pre-renal azotemia, 2. Renal azotemia, 3. Post-renal azotemia

Azotemia associated with biochemical and systemic clinicopathological alterations

Heavy proteinuria, hypo-albuminemia, severe edema, hyperlipidemia, lipiduria

Acute onset of gross hematuria, mild to moderate proteinuria, azotemia, edema, hypertension

Manifestation of mild glomerular abnormalities

Recent onset of oliguria or anuria with azotemia

Prolonged symptoms and signs of uremia

Bacteriuria and pyuria

Increased incidence of transitional-cell carcinoma of the renal pelvis or bladder

Acute renal failure due to necrosis of tubular epithelial cells

Hereditary, Developmental but nonhereditary, Acquired disorders

Acute DIN and Analgesic Nephropathy

Multiple expanding cysts of both kidneys that destroy the intervening parenchyma

Increased urine concentration of the stone's constituents (supersaturation)

Calcium oxalate, Calcium oxalate mixed with calcium phosphate, Magnesium ammonium phosphate, Uric acid, Cystine

Acute nephritic syndrome

Nephrotic syndrome

Acute renal failure

Prolonged symptoms and signs of uremia

Multiple cysts in both kidneys

Minimal-Change Disease (MCD)

P-fimbriae and type 1 fimbriae

Deposition of IgA immune complexes in the mesangium

1. Endogenous antigens (e.g., in SLE) 2. Exogenous antigens (e.g., bacterial, viral, parasitic infections) 3. Unknown antigens (e.g., membranous nephropathy)

Activation of complement, recruitment of neutrophils and monocytes, release of proteases, oxygen-derived free radicals, and arachidonic acid metabolites.

Anti-GBM antibody GN (Goodpasture syndrome)

Massive proteinuria, hypoalbuminemia, generalized edema, hyperlipidemia, and lipiduria.

Renal colic, hematuria, recurrent stone formation.

Effacement of podocyte foot processes associated with proteinuria.

Reduction in GFR, progression to end-stage renal failure, development of proteinuria, and glomerulosclerosis.

Glomerular, Tubular, Interstitial, Vascular.

Due to a T-cell derived factor that causes podocyte damage.

Minimal-Change Disease (MCD).

Types include primary (idiopathic) FSGS and secondary FSGS seen with various conditions.

Infections, malignancy, autoimmune diseases, exposure to inorganic salts, and certain drugs.

GBM thickening and proliferation of glomerular cells.

Clinical complex with acute onset, hematuria, oliguria with azotemia, and hypertension.

Associated with streptococcal infection, immune complex deposition, and low serum complement levels.

Deposition of IgA in the mesangium activating the alternative complement pathway.

Vesicoureteral reflux (VUR)

Drugs act as haptens that bind to a cytoplasmic or extracellular component of the secreting tubular cells and become immunogenic.

Acute DIN is due to drugs acting as haptens causing immunogenicity, while Analgesic Nephropathy is due to the intake of large quantities of analgesics.

The renal vasculature is secondarily involved in almost all kidney diseases, various forms of systemic arteritis involve renal vessels, and the kidney plays a role in hypertension pathogenesis.

ADPKD is characterized by multiple expanding cysts of both kidneys that ultimately destroy the intervening parenchyma.

The majority of renal stones (80%) are composed of either Calcium oxalate or Calcium oxalate mixed with calcium phosphate.

Increased urine concentration of the stone's constituents (supersaturation) is the most important cause of calcium stones formation.

Cystic kidney diseases are important as they are common, often present diagnostic challenges, and can be a major cause of chronic renal failure.

Deposition of IgA in the mesangium

Purpuric rash, abdominal pain, arthritis

Rapidly progressive loss of renal function, nephritic syndrome, severe oliguria, death from renal failure if untreated

Symmetrically contracted kidneys with red-brown surface

Inflammatory diseases involving the interstitium and tubules

Bacteria reach the kidneys through the bloodstream or ascending infection, leading to inflammation.

Due to factors facilitating bacterial entry to the bladder, such as short urethra and proximity to rectum.

Bacterial adhesion to urothelium and access to bladder, followed by outflow obstruction and urine stasis.