340 Tubulointerstitial Diseases of the Kidney Flashcards
Classic presentation of Acute Interstitial Nephritis (AIN)
- Fever
- Rash
- Peripheral eosinophilia
- Oliguric renal failure after 7-10 days of treatment with Methicillin or another Beta lactam antibiotic
NSAID-induced AIN
Acute renal failure with HEAVY PROTEINURIA
Rare: Fever, rash, eosinophilia
Therapeutic Agents responsible for AIN
- Antibiotics (B lactams, sulfonamides, quinolones, vanco, erythro, linezolid, minocycline, rifampin, ethambutol, acyclovir)
- NSAIDS, COX-2 inhibitors
- Diuretics (rarely thiazides)
- Anticonvulsants (Phenytoin, Valproate, Carbamazepine, Phenobarbital)
- Others: PPI, H2 blockers, captopril, mesalazine, allopurinol
Urinalysis in AIN
Pyuria
White blood cell casts
Hematuria
Allergic Interstitial Nephritis Diagnosis
Unexplained renal failure with or without oliguria PLUS exposure to potentially offending agent
Allergic Interstitial Nephritis Treatment
- Discontinue offending agent
2. Glucocorticoids may accelerate renal recovery and impact long-term renal survival (reserve for severe cases)
Systemic autoimmune disorder that primarily targets the exocrine glands (lacrimal and salivary) resulting in dry eyes and mouth (“sicca syndrome”)
Sjogren’s syndrome
Most common renal manifestation of Sjogren syndrome
Tubulointerstitial nephritis with predominant lymphocytic infiltrate
Diagnosis of Sjogren’s syndrome
- Positive anti-Ro (SS-A) antibodies
2. Positive anti-La (SS-B) antibodies
Treatment of Sjogren’s syndrome
- Glucocorticoids
2. Maintenance: Azathioprine OR mycophenolate mofetil (prevent relapse)
Hallmark features of Tubulointerstitial Nephritis with Uveitis (TINU)
Lymphocyte-predominant interstitial nephritis WITHharac painful anterior uveitis (often bilateral) AND accompanied by blurred vision and photophobia
Characteristics of TINU
- Unknown etiology
- 5% of all cases of AIN
- Females affected 3x more than males
- Median age of onset is 15 years
- Extrarenal features: fever, anorexia, weight loss, abd pain, arthalgia
- Others: Sterile pyuria, mild proteinuria, features of Fanconi’s syndrome, elevated ESR
Treatment for TINU
- Oral glucocorticoids
2. Maintenance: Methotrexate, Azathioprine, Mycophenolate mofetil (prevent relapse)
ABSOLUTE indications for corticosteroids and immunosupresives in intersitial nephritis
(Table 340-2)
- Sjogren’s syndrome
- Sarcoidosis
- SLE interstitial nephritis
- Adults with TINU
- Idiopathic and other granulomatous interstitial nephritis
RELATIVE indications for corticosteroids and immunosupresives in intersitial nephritis
(Table 340-2)
- Drug-induced or idiopathic AIN WITH: rapid progression of renal failure; diffuse infiltrates on biopsy; impending need for dialysis; delayed recovery
- Children with TINU
- Postinfectious AIN with delayed recovery
Type of AIN with renal biopsy revealing more chronic inflammatory infiltrate with granulomas and multinucleated giant cells and wherein tuberculosis should be ruled out before treatment
Granulomatous Interstitial Nephritis
Form of AIN with dense inflammatory infiltrate containing IgG4-expressing plasma cells and variably presents with autoimmune pancreatitis, sclerosing cholangitis, retroperitoneal fibrosis and chronic sclerosing sialadenitis
IgG4-related Systemic Disease
Cause of oliguric renal failure in acute urate nephropathy
Acute tubular obstruction
Uncommon but serious complication of oral Phospho-soda
Acute phosphate nephropathy
Should be avoided in pt with CKD
Calcium phosphate crystal deposition in tubules and interstitium
Acute renal failure in patients with multiple myeloma in the setting of hypovolemia, infection or hypercalcemia, or after exposure to NSAIDs or radiographic contrast media
Light chain cast nephropathy (LCCN) / “Myeloma kidney”
Characteristic of LCCN
Filtered monoclonal Ig light chains (Bence-Jones proteins) form intratubular aggregates with secreted Tamm-Horsfall protein in distal tubule
Goals of treatment for LCCN
- Correct precipitating factors (hypovolemia, hypercalcemia)
- Discontinue potential nephrotoxic agents
- Treat underlying plasma cell dyscrasia
* Plasmapharesis to remove light chains is questionable
Consequence of vesicoureteral reflux or other urologic anomalies in early chilfhood
Reflux nephropathy
Previously: Chronic pyelonephritis
Abnormal retrograde urine flow from the bladder into one or both ureters and kidneys because of mislocated and incompetent ureterovesical valves
Vesicoureteral reflux
Major causes of papillary necrosis
Table 340-3
- Analgesic nephropathy
- Sickle cell nephropathy
- Diabetes with urinary tract infection
- Prolonged NSAID use (rare)
Results form long-term use of compound analgesic preparations containing phenacitin, aspirin, and caffeine
Analgesic Nephropathy
Nephropathy due to aristolochic acid that includes Chinese herbal nephropathy and Balkan endemic nephropathy
Aristolochic Acid Nephropathy
Definitive diagnosis of Aristolochic Acid Nephropathy
Two of the following:
- Characteristic histology on kidney biopsy
- Confirmation of aristolochic acid ingestion
- Detection of aristolactam-DNA adducts in kidney or urinary tract tissue
Most common nephropathy in patients with manic-depressive illness treated with lithium salts
Nephrogenic diabetes insipidus
Mechanism: lithium accumulates in principal cells of collecting duct thru epithelial sodium channel (ENaC)
Triad of lead intoxication
- “Saturnine gout”
- Hypertension
- Renal insufficiency
Distinctive feature of gouty nephropathy histologically
Presence of crystalline deposits of uric acid and monosodium urate salts in kidney parenchyma
Most striking defect in hypercalcemic nephropathy
Inability to maximally concentrate urine
Due to reduced collecting duct responsiveness to arginine vasopressin and defective transport of sodium and chloride in loop of Henle
