Drug-induced acute tubulointerstitial nephritis: a case with elevated urinary cadmium

Abstract

Acute tubulointerstitial nephritis (ATIN) has many different causes, but is most frequently caused by drugs. We report a 13-year-old vegetarian girl with drug-induced ATIN, confirmed by renal biopsy, and simultaneous occurrence of elevated urinary cadmium. Four weeks prior to admission she had been treated with antibiotics and acetaminophen for respiratory infection, and remaining febrile, was treated with different "home-made" herbal mixtures. She presented with acute non-oliguric renal failure, tubular dysfunction, and sterile pyuria, but without skin rash or edema. Laboratory data showed a raised erythrocyte sedimentation rate, normal white blood count with eosinophilia, and a serum creatinine of 245 micromol/l. Urinalysis was remarkable for glycosuria, tubular proteinuria, and elevated beta(2)-microglobulin and N-acetyl-beta-D-glucosaminidase excretion. Immunoserological tests characteristic of acute glomerulonephritis and systemic diseases were negative. She was treated with steroids and her renal function improved. Follow-up analyses disclosed normal urinary cadmium and enzyme excretion within 6 months. Heavy metal analysis of herbal preparations that she had taken confirmed the presence of cadmium, but within approved concentrations. In conclusion, elevated urinary cadmium in the case of drug-induced ATIN may be assumed to be an accidental finding. However, consumption of different herbs containing cadmium and cadmium-induced nephro-toxicity could be the reason for such serious renal damage.

Acute Tubulointerstitial Nephritis due to Phenytoin: Case Report

“…It shall always be suspected in patients who show a sudden increase in levels of serum creatinine without apparent cause Perazella, 2014 [18]. The use of corticoids remains shrouded in controversy, but has been widely used in cases with important deterioration of kidney function, and has shown favourable results [4,17]. Therefore, the corticoid should be started promptly after the diagnosis of drug-induced ATIN is established to avoid the progressive replacement of interstitial cellular in iltrates by interstitial ibrosis [17].…”

“…It was considered that the AKI could have originated from medication secondary to the use of phenytoin, which, according to some previous related cases, could lead to nephrotoxicity [8,[12][13][14][15][16]. This means that the drug was immediately stopped and, due to the steady worsening of renal function, therapy based on corticosteroids was then promptly started [4,5,17,18].…”

“…Acute tubulointerstitial nephritis (ATIN) is an important cause of AKI, characterised, from the anatomopathological standpoint, by an interstitial in iltrate of mononuclear cells and eosinophils [4,5]. The classical clinical presentation of cases of ATIN includes the following key signs and symptoms: fever, skin rash, eosinophilia, and non-oliguric kidney failure, together with tubular dysfunction and abnormalities in the urinary sediment [4].…”

“…The classical clinical presentation of cases of ATIN includes the following key signs and symptoms: fever, skin rash, eosinophilia, and non-oliguric kidney failure, together with tubular dysfunction and abnormalities in the urinary sediment [4]. However, most cases proceed with non-speci ic symptoms, only followed by insidious deterioration of kidney function [6][7][8].…”

A brief study of toxic effects of some medicinal herbs on kidney

“…It carries serious risks since it removes calcium and iron and other nutrients from the body. [45] Dietary factors affect heavy metal uptake. For example, an adequate level of dietary iron reduces uptake of cadmium and lead.…”