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Interstitial Nephritis
Symptoms
▪ Often initially asymptomatic
▪ Arthralgia
▪ Hematuria (gross hematuria is rare)
▪ Nausea and vomiting
▪ Malaise
▪ Anorexia
Signs
▪ Fever
▪ Rash
▪ Oliguria
Patients with drug-induced AIN may have signs and symptoms of an allergic process, e.g. rash, fever, eosinophilia (although these are absent in NSAID-induced AIN)
▪ Urinalysis typically reveals moderate to minimal proteinuria (except in nonsteroidal anti-inflammatory drug (NSAID)-induced acute interstitial nephritis (AIN), in which proteinuria may reach nephrotic range), sterile pyuria, absence of red blood cell casts, and frequently eosinophiluria, but none of these findings are pathognomonic
▪ 50-70% of cases resolve on withdrawal of the causative agent within 7-10 days, and most (70%) make a good recovery
▪ Some patients (20-30%) have residual renal impairment, and may progress to end-stage renal failure
▪ Characteristically, patients present with a sudden deterioration in renal function (often with oliguria) several days to weeks after the introduction of a new medication
▪ Patients with drug-induced acute interstitial nephritis (AIN) may have signs and symptoms of an allergic process, e.g. rash, fever, eosinophilia, but these may be absent in more than half of all cases
Common causes
AIN may be drug-induced (85% of cases). Common drugs associated with AIN include:
▪ NSAIDs (including COX-2 inhibitors), proton pump inhibitors, ciprofloxacin, 5-aminosalicylates, penicillin, methicillin, rifampin, cephalosporins, trimethoprimsulfamethoxazole, thiazides, furosemide, triamterene, allopurinol, phenytoin, captopril, and cimetidine
AIN may be infection-induced. Infections associated with AIN include:
▪ Streptococcus, Legionella, Corynebacterium diphtheriae, Yersinia, Salmonella, HIV, Epstein-Barr virus (EBV), cytomegalovirus (CMV), Rickettsia, and Mycobacterium tuberculosis
Summary of Therapies
All treatments are given under the supervision of a nephrologist:
▪ Withdrawal of any offending medication: in 50-70% of patients in which the offending medication is withdrawn, resolution of the condition may begin within 7-10 days
▪ Corticosteroids: a trial of a corticosteroid, such as prednisone, should be considered if there is no improvement within 7-10 days after withdrawal of a medication thought to be responsible. Prior to initiation of corticosteroid therapy, a renal biopsy must be performed to confirm the diagnosis of acute interstitial nephritis (AIN) and to rule out the presence of significant degrees of interstitial fibrosis. If present, fibrosis contraindicates the use of immunosuppressive medications such as corticosteroids and cyclophosphamide, because these agents are ineffective in the presence of fibrosis, and they have serious adverse effects. Corticosteroids should be avoided in patients with active infection. Patients treated with corticosteroids should notice some improvement within 1-2 weeks, in which case the medication should be continued for 8-12 weeks with gradual tapering of the dose. If no improvement is noted in the first 2 weeks, the addition of cyclophosphamide might be considered upon recommendation and supervision by the consulting nephrologist
Prednisone Oral:
▪ 1mg/kg/day given in four divided doses
▪ Alternate regimen: 2mg/kg/day given every other day
▪ Treatment course: 8-12 weeks
▪ Cyclophosphamide: a second-line treatment; may be superimposed on the corticosteroid regimen (if renal biopsy shows little or no interstitial fibrosis) for a total treatment period not to exceed 2-3 months. If no improvement is seen, the medications should be stopped after 6 weeks
Differential Dx
Tubular necrosis:
Patients present with acute renal failure of sudden onset, and may develop oliguria, in a similar fashion to patients with AIN. However, patients with ATN usually have a history of a severe renal insult, such as prolonged hypovolemia or sepsis. On urinary microscopy eosinophiluria is not seen.
Features
▪ History of renal insult
▪ Many patients develop oliguria
▪ Urine sediment contains muddy brown casts and tubular epithelial cells
▪ intrinsic renal failure is most commonly associated with acute tubular necrosis (ATN) following severe systemic insult, e.g. surgery, trauma, burns, hypotension, sepsis
Symptoms
▪ May rarely be asymptomatic
▪ Lethargy, weakness
▪ Anorexia
▪ Nausea and vomiting
▪ General malaise
▪ Muscle cramps
▪ Decreased consciousness
Coma
Delirium or confusion
Drowsy, lethargic, hard to arouse
▪ Decreased urine output or no urine output
▪ General swelling, fluid retention
Nausea, vomiting
Signs
▪ Skin pallor
▪ Ecchymoses
▪ Peripheral edema
▪ Tachypnea
▪ Tachycardia
▪ Confusion
▪ Seizures
▪ Oliguria or anuria
▪ Pulmonary rales secondary to volume overload
▪ Arrhythmias secondary to hyperkalemia and severe acidosis
▪ Asterixis or flapping tremors
▪ Uremic fetor
Treatment
▪ aggressive fluid resuscitation to restore intravascular volume may reduce incidence of acute tubular necrosis (ATN)
▪ Judicious use of a diuretic such as furosemide often converts an anuric or oliguric patient to a nonoliguric patient, and makes the management of the patient easier; however, the prognosis of the acute renal failure does not change
▪ Dietary modification may be necessary in ATN to provide adequate calories while minimizing accumulation of toxins by moderate short-term protein restriction. Prolonged protein restriction is inadvisable and may delay recovery
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