Intrinsic Acute Renal Failure
Causes of Intrinsic Acute Renal Failure
Tubulointerstitial diseases
Hypersensitivity reactions to medications: PCN, sulfonamides, fluoroquinolones, chemotherapeutic agents, NSAIDs
Light chains in multiple myeloma
Autoimmune processes: Sarcoidosis, Sjogren's synd, lymphoma.
Associated with infections: Legionella, Toxoplasma, CMV, EBV
Exposure to organic solvents
Pyelonephritis
Glomerular diseases
Nephrotic syndrome: Most commonly occurs in children and results from significantly increased basement membrane permeability with heavy or nephrotic range proteinuria, >3.5 g/day. Nephrotic range proteinuria is often glomerular in nature. Excreted primarily as albumin. Hypoalbuminemia decreases oncotic pressure and may be expressed as fluid accumulation in interstitial tissues: periorbital and facial edema, peripheral edema, anasarca, pleural effusions, and ascites. BP is usually normal. HLP and lipiduria occur secondary to increased hepatic production and impaired clearance. Mild hematuria can occur, but often the basement membrane has enough integrity to trap RBCs. Nephrotic synd. is associated with hyperocoagulable state; the most common being thromboembolic complications including renal vein thrombosis.
Minimal change disease
does not progress to chronic renal failure
FSGS
Immunoglobulin and complement deposition detected by immunofluorescence
Membranous nephropathy
Rule of thirds for membranous GN: One third progress to CRF, one third have spontaneous remission, one third remain nephritic and do not progress.
Caused by immune complex deposition
Idiopathic, SLE, Hep-B
Diabetic nephropathy (diffuse glomerulosclerosis, nodular glomerulosclerosis)
Nephritic syndrome: clinical definition involves abrupt onset hematuria with RBC casts, mild proteinuria, often included HTN, edema, and azotemia. Nephritic synd represents inflammatory responses characterized by glomerular capillary damage and rupture leading to edema, hematuria with dysmorphic RBCs, mild to moderate proteinuria <3.5 g/day, HTN, and uremia. Variable renal insufficiency may develop with azotemia and oliguria. If RBCs are trapper in the urinary casts, bleeding probably originated in the nephron and nephritic synd is more likely; RBC casts are an indication of glomerulonephritis.
RPGN
Also called crescentic GN
Pauci-immune GN: 50% of RPGN where no immune
PSGN
Inf with nephritogenic strains of group A beta hemolytic streptococcus (usually associated with preceding pharyngitis or impetigo)
Immune complex deposition with complement (IgG, C3, C4) in a granular pattern
10 - 30% adults and 1% children will develop RPGN
24-h protein usually between 0.5 - 2 g/day
RBC casts in urine
ASO positive within 1 - 2 weeks in post pharyngitis PSGN
Hypocomplementemia of C3 and C4 during active phase, returning to normal within 6 weeks. If PSGN is membranoproliferative type, complement level will not return to normal.
IGA nephropathy
Membranoproliferative GN
Postinfectious glomerulonephritis
Focal glomerulosclerosis associated with AIDS
Secondary (multisystem associated) glomerular diseases
Collagen vascular disorders
PAN
SLE
Wegener's granulomatosis
Henoch-Shonlein purpura
Hematologic disorders:
TTP
HUS
serum sickness
Glomerular basement membrane disease
Alport's syndrome
Goodpasture's syndrome
Thin basement membrane disease
Acute tubular necrosis
Ischemia, hypotension, septicemia, postoperative patients
Direct drug toxicity:aminoglycosides, cisplatin, amphotericin, contrast agents, cyclosporine
Myoglobin or hemoglobin
Renal cortical necrosis
ATN in pregnancy
Hypercalcemia
Vascular disease
Renal artery occlusion
Acute vasculitis
Malignant HTN
Atheroembolic disease, multiple cholesterol emboli syndrome