Tubulointerstital Diseases Flashcards
Two most common causes of acute tubular necrosis
Acute loss of Bloodflow (trauma, acute pancreatitis, shock, sepsis)
Nephrotoxic Agents
Most commonly mentioned nephrotoxic agents that trigger acute tubular necrosis
Gentamicin/Other ABs
Contrast
Heavy Metal
Organic Solvents (Carbon Tetrachloride)
Less common causes of acute tubular necrosis
Ethylene glycol/Methanol poisoning
Hemaglobinuria/Myoglobinuria (crush injury, OH binges)
acute tubular necrosis casts are made primarily of
Tam Horsfall protein
Can also add globin + plasma proteins
Describe the appearance of regenerating epithelial cells in acute tubular necrosis
Flattened
Hyperchromatic Nuclei
Mitotic Figures
Carbon tetrachloride poisoning microscopic features
Neutral lipid accumulations
Ethylene glycol poisoning microscopic features
Ballooning and hydrophobic or vacuolar degeneration with formation with formation of Ca Oxalate Crystals
Describe the three clinical phases of acute tubular necrosis
- Initiating - Slight decline in urine output + inc. BUN
- Maintenance - Major drop in renal output, too much salt, water, BUN, K, and metabolic acidosis
- Recovery - Steady increase in urine output, hypokalemia risk
Describe the features of acute tubulointerstitial nephritis
- Interstitial edema, leukocytic infiltrates, focal tubular necrosis
- Caused by acute renal failure
Describe the features of chronic tubulointerstitial nephritis
- Infiltration by mononuclear cells, interstitial fibrosis, and tubular atrophy
- Caused by slowly progressing toxic damage (analgesic abuse)
- Usually not recognized till late
How is tubulointerstitial nephritis clinically distinguished from other renal diseases
ABSENCE of nephrotic/nephritic symptoms
Impaired concentrating ability
Salt Wasting
Metabolic Acidosis
Drugs that cause Acute interstitial nephritis
- Sulfonamides, Synth. Penicillins, other synt. ABs (rifampin)
- Diuretics (esp. thiazides)
- NSAIDs (phenylbutazone)
- Pheniodine and cimetidine
Clinical presentaiton of a hypersensitivity rxn triggered interstitial nephritis
2-6 weeks after drug exposure
Fever, Eosinophilia, Rash, Renal abnormalities
Acute renal failure in 50%
Describe the process of developing chronic renal disease due to analgesic abuse
First – Papillary Necrosis, tubulointerstitial neph. is 2dary
NSAID covalently binds and oxidatively damages
Inhibit PGs –> No Vasodilation –> Papila ischemic
Which analgesics are most prone to cause chronic renal disease due to analgesic abuse
Phenacetin
Aspirin, Caffeine, Acetaminophen, Codeine
Clinical associations for interstitial nephritis from analgesics
- Look for women with chronic headaches, pains
- Early – cant concentrate urine, acidosis, stones
- UTI in about 50%
Causes of papillary necrosis
Analgesic nephropathy Diabetes Urinary Tract Obstruction Sickle Cell Renal TB
Cancer that chronic analgesic abuse is associated with
transitional papillary carcinoma of the renal pelvis
NSAID drug nephropathy is associated with which glomerular disease
membranous glomerulonephritis
Three forms of urate nephropathy
- Acute Urate Nephropathy 2dary to uric acid crystals
- Chronic urate nephropathy
- Nephrolithiasis w/ uric acid stones
Important details abut acute urate nephropathy secondary to precipitation of uric acid crystals
Obstructs nephrons/CDs
Can cause Acute Renal Failure
Assocaited with Leukemias and Lymphomas going thru chemo
Disorders that cause hypercalcemia (4)
Hyperparathyroidism
Multiple Myeloma/Bone Cancer
Vitamin D intoxication
Taking in too much Ca
What happens to the Bence Jones (light chain) proteins the kidney of a multiple myeloma patient
Proteinuria + Cast nephropathy
Light chains are toxic to epithelial cells
Combine with Tamm-Horsfall to make casts
Cause obstructions with peritubular inflammation**
Other than the Myeloma kidney with peritubular inflammation, what are some other ways that multiple myeloma may affect kidney fxn
Amyoidosis
Light Chain Glomerulonephritis
UT obstruction with secondary pyelonephritis
