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Renal System- Interstitial Tubular & Disorders by Ryan
Renal System- Interstitial Tubular & Disorders by Ryan
Acute Interstitial Nephritis is...and what does it present with?
-Drug-induced hypersensitivity
-Often presents with EOSINOPHILIA
-Urine sediment varies from GNs
-Does NOT have heavy albuminuria, RBC casts or fat bodies
-May have eosinophils, RBCs, WBCs & WBCs casts
-Also have beta-2-microalbuminuria
Common culprits:
-Antibiotics (methicillin, TMP/SMX, Rifampin)
-NSAIDs
-Cimetidine (H2 blocker)
-Thiazides
-Phenytoin (anti-convulsant)
-Allopurinol

Antibiotic Induced AIN
-Also fluoroquinolones (rarely given to kids)
-Cause the classic triad of fever, rash, and eosinophils
-Idiosyncratic response to antibiotic
-Not related to dose or duration
What may you possibly not see with NSAID induced AIN?
-Usually need to take NSAIDs for months before symptoms occur
-Rash, fever & eosinophilia may NOT occur
-Often nephrotic range proteinuria with minimal glomerular changes
Which systemic diseases can give you AIN?
-Sarcoidosis
-SLE
-Infection (pyelonephritis)
-Transplant rejection
Chronic interstitial nephritis etiologies?
-Renal outlet obstruction
-Drugs
-Chronic analgesic abuse, cisplatin, cyclosporin
-Heavy metals
-Especially lead & cadmium
-Sjogren disease
-Sickle cell disease
What does CIN present with?
-Consider in a patient with a history of frequent pain who presents with proteinuria & elevated creatinine
-Check for lead toxicity in kids
-Consider in a patient who has glucosuria with normal serum glucose
-NSAIDs can cause either acute or chronic interstitial nephritis
Renal tubular acidosis
-Metabolic acidosis usually caused by a defect in renal tubular function
-Often genetic
-One proximal type (type 2) & two distal types (1 & 4)
-ALL RTAs have a normal anion gap
-Number indicates the serum K+ level
-1 is low, 2 normal, 4 is high
What causes Type 2 RTAs?
-Causes by a mechanism similar to acetazolamide
-Decreases bicarbonate resorption in the proximal tubule
-In children, frequently caused by Fanconi SYNDROME
-NOT FANCONI’S ANEMIA
What are common etiologies of type 2?
-Fanconi Syndrome
-Drugs
-Acetazolamide & 6-mercaptopurine
-Heavy Metals
-Lead, copper, mercury, cadmium
-Disorders of protein, carbohydrate, or amino acid metabolism
-Multiple myeloma (in adults)
Wait, so what is Fanconi Syndrome?
-Rare disorder of tubule function
-Results in excess amounts of glucose, bicarbonate, phosphates (phosphorus salts), uric acid, potassium, sodium, and certain amino acids being excreted in the urine.
-May be hereditary
-Also exposure to heavy metals, chemicals, vitamin D deficiency or a systemic disorder
What do Type 4 RTAs affect?
Affects the Na/K-H exchange in the distal tubule
-Effect similar to spirinolactone or hypoaldosteronism
-Hyperkalemic, hyperchloremic acidosis
Common etiologies of Type 4?
-Obstructive uropathy*
-Interstitial renal disease*
-Multicystic dysplastic kidneys*
-Type 1 pseudoaldosteronism
-Diabetic nephropathy
-21-hydroxylase deficiency
-Renal transplant

*common in kids
How do you treat Type 4 RTAs
Treatment is aimed at treating the primary disease

Can try to give NaHCO3, but you MUST restrict potassium
What is the defect in Type 1?
Also a distal defect, but only a defect in H+ secretion
-Patients become acidotic & HYPOkalemic

Children commonly present with failure to thrive

Commonly causes renal stones
-Likely from decreased citrate excretion and hypercalcuria
Common etiologies of Type 1
-Amphotericin B (antifungal)
-Toluene (glue sniffing)
-Lithium (Bipolar medication)
-SLE
-Sjogren’s
-Chronic active hepatitis