Interstitial nephritis acute kidney injury

Acute kidney injury may be due to tissue parenchymal injury as manifested by direct tubule toxicity, acute interstitial nephritis, osmotic nephrosis and thrombotic microangiopathy. 

Acute kidney injury with eosinophihc interstitial nephritis was attributed to abacavir in one patient with HIV infection who also had what appeared to be "classic" FSGS on renal biopsy [83]. The serum creatinine returned to baseline levels after treatment with prednisone and discontinuation of abacavir. 

Other protease inhibitors have also been rarely associated with kidney injury. A single case of interstitial nephritis and reversible AKI in a patient treated with atazanavir has also been reported [153] Acute kidney injury attributed to ritonavir has been reported in several patients [154-157], the majority of whom were receiving concomitant nephrotoxic medications, while others had preexisting kidney disease or were volume depleted. In several patients, AKI recurred upon ritonavir rechallenge. Kidney biopsies were not performed, so histopathologic correlates and etiology of kidney injury were not precisely defined. 

Amphetamines are sympathomimeticamines with central nervous system stimulatory activity. They may induce a number of patterns of renal damage including rhabdomyolysis related acute kidney injury, acute interstitial nephritis and an angiitis resembling polyarteritis nodosa. 

Amphetamines have also been associated with a syndrome of acute kidney injury and rhabdomyolysis. Several series have described patients following intravenous injection of methamphetamine or phenmetrazine who presented with hyperactivity, fever, chills, sweats, abdominal cramps, diarrhea, and hypotension [177,178]. The patients have developed acute kidney injury which is usually oliguric and associated with classic rhabdomyolysis, similar to cases of cocaine-induced rhabdomyolysis. Several patients have had disseminated intravascular coagulation and liver function abnormalities as well. Methamphetamine abuse has also been associated with accelerated hypertension, unexplained chronic renal failure, acute lead poisoning (a common reagent used in its production utilizes lead acetate) and at least one case of biopsy proven interstitial nephritis the latter patient responded to intravenous corticosteroids but whether the nephritis was truly due to amphetamines remains unproven [179]. 

Acute kidney injury has also been associated with a variety of sedatives and hypnotics including barbiturates, benzodiazepines, glutethimide and dilorpro-mazine [107,108,119]. The acute kidney injury is usually related to rhabdomyolysis but the classical clinical picture of acute interstitial nephritis has been reported in one patient with the use of diazepam, although no renal biopsy was performed [186]. In fhose patients with rhabdomyolysis, multiple seizures often develop prior to the rhabdomyolysis and others are febrile at the time. However, the most common presentation is that of a young person without a prior medical history who presents with coma-stupor of one to several days duration, variable signs of volume depletion, limb compression and follows the typical course of acute tubular necrosis with a high likelihood of renal recovery [107-109]. 

Urinary tract In a case-control study the risk of acute interstitial nephritis (AIN) and acute kidney injury (AKI) was estimated for exposure to nonselective NSAIDs (nsNSAIDs), (proton pump inhibitors) PPIs and co-exposure to both (nsNSAID + PPI). There were 68 AIN cases identified from a primary care database from the United Kingdom (Clinical Practice Research Datalink) who were matched to 3347 controls. The risk of AIN for use of PPIs only was 3.2 (95%CI 0.8-12.8), of nsNSAIDs only was 1.9 (95%CI 0.7-5.5) (Cl, confidence interval). For individual nsNSAIDs diclofenac showed an odds ratio (OR) of 2.7 (95%CI 0.6-10.9) piroxicam provided an OR of 28.0 (2.2-365.1), however, the estimates are affected by the small number of cases and matched controls. Regarding AKI (n=27,982 cases n= 1,323,850 matched controls), the risk was increased by 31% for use of nsNSAIDs only (OR 1.31 95%CI 1.25-1.37) and for nsNSAIDs + PPI by 33% (OR 1.33 95%CI 1.07-1.64) [2 =]. 

Leonard CE, Freeman CP, Newcomb CW, Reese PP, HerUm M, Bilker WB, et al. Proton pump inhibitors and traditional nonsteroidal anti-inflammatory drugs and the risk of acute interstitial nephritis and acute kidney injury. Pharmacoepidemiol Drug Saf November 2012 21(ll) 1155-72. 

Interstitial nephritis has been found in kidney biopsies in patients treated with indinavir [146-151]. Some of these cases have described eosinophiluria and crystals (assumed to be indinavir) associated with histiocytes and giant cells in the renal tubules. Some of these patients were asymptomatic, while others reported classic symptoms of nephrohthiasis. Cortical atrophy was found in some patients, suggesting the progression from acute injury towards chronic kidney disease [152]. 

The interstitium of the kidney is also susceptible to injury from a variety of causes. Although acute interstitial nephritis is most commonly caused by medications (see Chap. 46), infections (e.g., streptococcal, leptospirosis, hantavirus, and human immimodeflciency virus), selected autoimmune disorders (systemic lupus erythematosus or mixed connective tissue disease) also may produce a similar syndrome. The presence of white blood cells (WBCs), WBC casts, and coarse granular casts in the urine aU suggest interstitial inflammation. The presence of eosinophUia and eosinophiluria also strongly suggest the presence of an interstitial nephritis. Occasionally low to moderate proteinuria can be seen on urinalysis. 

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