ACUTE INTERSTITIAL NEPHRITIS

Acute interstitial nephritis classically presents with fever, maculopapular rash, eosinophilia, eosinophiluria, and urinary WBC casts.  Eosinophiluria is neither sensitive (sensitivity 40%) nor entirely specific (specificity 72%, positive predictive value 38%).  The classic triad of rash, fever and eosinophilia is actually uncommon and only seen approximately 10% of the time.  One can also see mild proteinuria (usually < 1g/d) and other signs of tubular damage, such as renal tubular acidosis and Fanconi’s syndrome. Renal ultrasound generally reveals kidneys of normal to large size. Gallium scanning has been suggested as an aid to distinguishing this condition from acute tubular necrosis (ATN).  It is negative in ATN but generally positive in interstitial nephritis. 

Drug classes that can cause AIN:

Penicillin analogs (methicillin, ampicillin, etc.)– most common

Cephalosporins

Sulfonamides (sulfamethoxazole,cotrimoxazole)

Other antibiotics such as rifampin andciprofloxacin

NSAIDS (including Cox-2 specific agents)

Diuretics

Proton pump inhibitors

Miscellaneous – this includes a very largenumber of drugs such as allopurinol and cimetidine.

Risks related with renal biopsy

The incidence of gross hematuria is approximately 5-10%

·        The incidence of significant bleeding enough to delay discharge is approximately1:100.  This refers to persistent hematuria, or perinephric hematoma, which usually settles with conservative management

·        A transfusion is occasionally necessary

·        Serious bleeding complications sufficient to warrant interventions to stop bleeding are of the order of 1:1000

·        Kidney biopsy can be life threatening in 1:5000-1:10000 

Nephrolog

Goodpasture’s disease is the most aggressive and rapidly progressive glomerulonephritis
encountered in clinical practice. Crescentic nephritis may be accompanied by lifethreatening
pulmonary hemorrhage.. Treatment with cyclophosphamide, steroids, and plasma exchange can arrest the
disease, but renal damage may be irrecoverabl
. In small-vessel vasculitis, the mainstay of therapy consists of corticosteroids and
cyclophosphamide.. In antineutrophil cytoplasmic autoantibody (ANCA) vasculitis, plasma exchange is
presently recommended in addition to corticosteroids and cyclophosphamide for
patients presenting with advanced renal failure and/or pulmonary hemorrhage.. A high rate of venous thromboembolism has been reported in ANCA vasculitis, with
about 10% of patients developing symptomatic events.


 

How to differentialte acute from Chronic renal failure?

In terms of history, onemust determine whether previous serum creatinines are available or if thereis any history of any systemic diseases that may be associated with renalinvolvement. Often, one must take the time to call otherphysicians or hospitals to get old creatinine values.

When it seems that one isdealing with acute renal failure then there needs to be an assessment forprerenal, renal or post-renal causes.

On physical examination, oneshould look for evidence of a pre-renal cause of renalinsufficiency. Hypovolemia would be suggested byfeatures of decreased extracellular fluid volume such as a low JVP, drymucous membranes or postural tachycardia or hypotension.Pre-renal disease can also be due to conditions such as congestiveheart failure or cirrhosis, so one should also perform a careful cardiacexam and look for stigmata of chronic liver disease.Post-renal failure can be seen in bladder outlet obstruction, so onecould feel for a palpable bladder. Intrinsic renaldisease can develop acutely due to systemic disease with renal involvement.One can look for features of some of these systemic conditions which mightinclude rashes, active joints, alopecia, oral/nasal ulcers, peripheralneuropathy, or a murmur from endocarditis.

In terms of lab data,urinalysis is critical. One may see casts that willhelpful in terms of diagnosis: RBC casts for glomerulonephritis, WBC castsin acute interstitial nephritis and heme granular casts in acute tubularnecrosis. In chronic renal disease, one may see waxy orbroad casts.

Chronic renal failure may alsobe associated with anemia, metabolic acidosis, hypocalcemia andhyperphosphatemia. These may not be entirely reliable,however, as anemia can develop acutely in patients with conditions such aslupus or vasculitis, and hypocalcemia/hyperphosphatemia can be seen inconditions such as tumour lysis syndrome.

On ultrasonography, smallkidneys with cortical echogenicity would suggest kidney disease ischronic. If kidney size is preserved this might suggestacute renal failure, though some diseases of the kidney are associated withpreservation of renal size (examples include diabetic nephropathy andamyloidosis).