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Lecture 4
Interstitial Renal Disease
Question | Answer |
---|---|
Definition of Acute Interstitial (Hypersensitivity) Nephritis | Acute renal failure with interstitial inflammatory cells (activated T-lymphocytes and/or eosinophils) and interstitial edema |
Main Causes of AIN? | Idiopathic, Drugs, Infection, Toxins, Immunologic Disease |
What are some Drugs that can cause AIN | NSAIDS, Methicillin, Some Antibiotics, and diuretics (furosemide and thiazide) |
What is the mechanism of AIN | Allergic hypersensitivity |
How long does it take AIN to develop | several weeks |
Definition of Chronic Interstitial Nephritis (CIN) | Chronic renal failure with mixed chronic inflammatory cell infiltrate in interstitium, tubular atrophy and fibrosis |
What is the mechanism for CIN | Physical or Chemical with precipitation of substances in the medulla or ischemic due to drug induced vascular changes |
What are the main causes of CIN | Drugs (NSAIDS, Analgesics, Lithium), Urinary Tract Obstruction, Kidney stones/infection, Polycystic Kidney Disease |
What is the gross pathology of CIN | asymmetrically scarred small shrunken kidneys, sometimes with papillary necrosis with NSAIDS/acetaminophen |
What is the most common bacteria responsible for Ascending infection in pyelonephritis | E. coli |
Define Pyelonephritis | Infection involving the parenchyma, calyces and pelvis |
Define Chronic Pyelonephritis | Multiple episodes of infection secondary to vicoureteral reflux with chronic renal damage or secondary to obstruction |
What is the gross pathology of chronic pyelonephritis | small kidneys with coarse scars, dilated papillae, parenchymal atrophy |
Define ATN (acute tubular necrosis) | Acute renal failure secondary to tubular damage |
What are the four main causes of ATN | Ischemic, Post-transplantation, Toxic, and Obstructive |
What are the three phases of ATN | Oliguric, Diuretic, Regenerative |
What makes someone predisposed to papillary necrosis | long term analgesic use, dibetic with pyelonephritis, and sickle cell anemia |
What is the etiology of calcium oxalate or phosphate kidney stones | idiopathic |
what is the etiology of struvite/magnesium ammonium phosphate kidney stones | Infection |
What are the three "urias" that can result in urolithiasis | Hypercalciuria, Hyperuricosuria, and cystinuria |
What are the kidneys like in patients with ADPKD (Autosomal Dominant Polycystic Kidney Disease) | very large cystic kidneys with round cysts of variable size and no dysplasia (all parts of nephron invoved and bilateral) |
Where else do you see cysts in pts with ADPKD | liver, spleen, pancreas (no effect on function) |
What are two other associated problems in patients with ADPKD (Cardiovascular) | Mitral valve prolapse (25%) and Cerebral Aneurysms (10-20%) |
How do the kidneys look in patients with ARPKD (autosomal recessive polycystic kidney disease? | Large smooth kidneys with narrow cysts perpendicular to the pasule and involving the collecting ducts |
What percent of patients on dialysis develop cysts after 5 years | 75% |
What disease results in translucent cysts on the surface of the cortex up to 10cm and is present in 50% of people >50 | Benign simple cystic disease |
What is the most common cause of an abdominal mass in newborns | Multicysitc renal dysplasia |
What are causes for Early Non-Function following Renal Transplantation | "Plumbing" problem, ATN, Acute Cellular rejection |
When does Acute Cellular Rejection typically occur | usually within the first 3 months |
How do you detect Acute Cellular Rejection | increasing creatinine |
What findings support the diagnosis of Acute Antibody Mediated Rejection | Fluorescent antibodies to C4d and Donor Specific Antibodies |
What is the most frequent cause of graft loss | Chronic Allograft Nephropathy |
What Renal Diseases can be recurrent after transplant | Type II Membranoproliferative GN, Diabetic glomerulosclerosis, IgA nephropathy, Focal Segmental Glomerulosclerosis |