Module 4: Renal: Tubular and Interstitial Diseases Flashcards
Before we get into the specific diseases lets talk about casts, what are they?
Indicates a problem in the glomerulus or tubules
- -made of Tamm-Horsefall proteins
- -casts take the shape of the tubules
What are the various types of casts?
Hyaline Casts: --physiological: only one from dehydration or exercise Granular (muddy brown): --acute tubular necrosis (hypovolemic shock or hypotension) Waxy: --chronic renal failure and broad based RBC cast: --nephritic syndrome WBC cast: --acute pyelonephritis (PMNs) and Allergic Interstitial Nephritis (Eosinophils) (following drugs, rash, and fever, and azotemia) Lipid Casts: --nephrotic syndrome WBCs in urine: --acute pyelonephritis or allergic interstitial nephritis or cystitis RBCs in urine --nephritic syndrome or bladder cancer Oval fat bodies: --nephrotic syndrome
When can you see casts in the urine below the kidneys?
Only if hydronephrosis is present
Now moving onto conditions of the tubes. What are the two major causes of acute tubular necrosis?
Ischemic and toxic
What are the predictable phases of acute renal failure?
Initiation Phase (36 hours)
–Acute decrease in GFR and rapid increase in serum creatinine and BUN
Maintenance Phase:
–Plateau of serum creatinine and BUN
–Lasts for days to 3 weeks (oliguria)
–Uremic symptoms, fluid overload, metabolic acidosis and hyperkalemia (requires dialysis)
Recovery Phase:
–Tubular function restored, increased GFR and increased urine volume
–gradual decrease in creatinine and BUN
What do you find in urine and on labwork for acute tubular necrosis?
Urine findings: muddy brown casts, epithelial casts, free epithelial casts, mild proteinuria, microscopic hematuria and no pyuria
Lab: Increased serum creatinine and BUN, metabolic acidosis, hyperkalemia, hyperphosphatemia and anemia (decreased EPO)
What is found on PE and histology for acute tubular necrosis?
PE: hypotension, oliguria and uremic symptoms
Histology: coagulative necrosis of the tubules
What are complications of acute tubular necrosis?
Ischemic Insult: hypotension, vasodilatory (septic shock) systemic infection, hemorrhagic shock (GI bleeding), hypovolemic shock (vomiting and diarrhea)
Nephrotoxic: Exogenous= aminoglycosies
and endogenous= hemoglobinuria and myglobinuria
Moving onto Tubulointerstitial Nephritis, what is the tubular dysfunction?
- -Impaired urinary concentration (polyuria, and nocturia)
- -Salt wasting (hyponatremia)
- -Metabolic acidosis (decreased ability to excrete acid)
- -No significant protenuia/hematuria
What is the etiology for tubulointerstitial Nephritis?
- Acute: drugs(abx), infection, idiopathic, and sarcoidosis
- -chronic: infection (pyleonephritis), analgesic abuse, urate nephropathy
any random facts?
ssds
Moving onto the next tubular syndrome is acute drug induced Interstitial Nephritis. What is the etiology?
Penicillin (Abx), cephalosporin, NSAIDs, sulfonamides, ciprofloxacin, rifampin, cimetidine, allopurinol, and proton pump inhibitors.
What is the pathogenesis for acute drug inducted interstitial nephritis?
Allergic type reaction manifested by interstitial infiltration of eosinophils, lymphocyte and macrophages
–onset 2 weeks after first exposure or 3-5 days if 2nd exposure
What is the presentation for acute drug induced interstitial nephritis?
Fever Rash Eosinophilia ARF Oliguria
What is seen on blood and urine for acute drug induced interstitial nephritis?
Urine: eosinophils, sterile, pyuria (without bacteria), WBC casts, proteinuria
Blood: Increased BUN and creatinine, increased eosinophils and tubular dysfunction (increased K and decreased HCO3)
What is the treatment for acute drug induced interstitial nephritis?
Stop using drug = complete recovery
Next topic for tubular pathology is acute pyelonephritis. What population do you see this in and why?
More common in females
–due to shorter urethra