INTERSTITIAL NEPHRITIS(IN)
الدكتور خلدون ذنون- كلية طب نينوى- المرحلة الرابعةObjectives
The following points warrants concentration:
1. Definition and causes of acute and chronic IN
2. NSAIDs is an important cause of IN.
3. IN may result in renal tubular damage.
4. Features of renal tubular damage.
5. IN may result in acute and even chronic renal failure.
6. Most important management is removal of the cause, which results even in reversal of renal failure.
7. Analgesic nephropathy, sickle cell nephropathy and reflux nephropathy
Acute interstitial nephritis AIN
Acute inflammation of tubulo-interstitium.Causes
Allergic: penicillin, NSAID, proton pump inhibitors, mesalazine.
Immune: SLE.
Infection: pyelonephritis, leptospirosis, T.B., CMV.
Toxic: myeloma light chain, mushroom.
Pathology
Inflammatory cellular infiltrate involving tubules & interstitium, sometimes eosinophils are prominent.
Presentation and diagnosis
Less than 30% of drug induced AIN have drug hypersensitivity e.g fever, rash, eosinophilia, leucocyturia is common, up to 70% demonstrate eosinophiluria.May present as ARF e.g ATN.
Many patients are not oliguric (non-oliguric ARF).
Proteinuria & albuminuria rarely >1gm/24hr, LMW protein is common e.g B2-microglobulin, lysozyme. Haematuria & pyuria are frequent.
Renal biopsy is usually required.
Management
Treat the cause e.g drug withdrawal.Conservative management of ARF.
Dialysis: b.uria >30mmol/L.
Steroid 1mg/kg/day accelerate recovery, (scarring.
Chronic interstitial nephritis (CIN)
CausesPersistent causes of AIN.
Glomerulonephritis may be associated with CIN.
Immune: SLE, sarcoidosis, sjogren syndrome, chronic transplant rejection.
Toxic: mushroom, lead, Chinese herbs, Balkan nephropathy.
Drugs: lithium, NSAID, ciclosporin, tacrolimus.
Infection: pyelonephritis.
Congenital: vesicoureteric reflux, Wilsons disease, sickle cell nephropathy.
Metabolic-systemic: hypokalaemia, hypercalciuria, amyloid.
Clinical features
Present in adult life as CRF, hypertension, small kidneys.
Hyperkalaemia & acidosis are prominent due to tubular dysfunction & hyporeninaemic hypoaldosteronism e.g diabetic nephropathy.
Minority present with salt losing nephropathy(Na & water depletion( polyuria & hypotension.
Renal tubular acidosis: myeloma, sarcoidosis, amyloidosis.
Urine exam.non specific: WBC, RBC, proteinuria<2gm/24hr.
Management
( Treat & eliminate the cause e.g drug, toxin, infection, SLE.
( Conservative management of CRF.
( Correct acidosis by oral Na bicarbonate.
( Correct hyperkalaemia.
ANALGESIC NEPHROPATHY
NSAID, phenacetin (withdrawn) ( acute&chronic IN( ARF& CRF.SICKLE CELL NEPHROPATHY
Renal papillary necrosis, chronic IN.REFLUX NEPHROPATHY
Congenital, frequent UTI, chronic IN, renal scarring, proteinuria, hypertension, CRF & renal calculi.Micturating cystourethrogram ( distended ureters & pelvi- calyces. U/S shows small kidneys due to renal scarring in the chronic conditions.