Delayed Renal Function Recovery From Drug-Induced Acute Interstitial Nephritis

ArticleinThe American Journal of the Medical Sciences 343(1):36-9 · December 2011with23 Reads
Impact Factor: 1.39 · DOI: 10.1097/MAJ.0b013e3182350362 · Source: PubMed

Acute interstitial nephritis, considered one of the major causes of reversible acute kidney injury, was frequently encountered as drug-treatment complication in the early stage of infection control. In some cases, drug-induced acute interstitial nephritis (DIAIN) resulted in delayed function recovery or chronic kidney disease. To study the underlying mechanism, the authors investigated the clinical and pathological features of DIAIN patients with delayed renal function recovery. The delayed recovery group consisted of patients with reduced renal function for more than 3 months after diagnosis. In this retrospective study, 18 patients with DIAIN from January 2003 to December 2009 were identified as the delayed recovery group, whereas 54 patients with DIAIN who recovered completely within 3 months were treated as the control group. Clinical and pathological features were compared between the 2 groups. In the delayed recovery group, the average age at onset was 48.8 years, antibiotics and herbs were the 2 main causative drugs and the dominant extra-renal manifestation was gastrointestinal symptomatology. In comparison with patients in the control group, patients in the delayed recovery group had longer interval time from disease onset to hospitalization, and they presented with less oliguria. Moreover, these patients had higher levels of urine retinol binding protein, and more renal interstitial inflammatory cell infiltrations were observed in their renal histology. Aging, long interval time from disease onset to hospitalization and renal interstitial inflammatory cell infiltration may predict delayed renal function recovery.

    • "The largest study disclosed that 60 out of 120,132 (0.05%) patients developed AKI [11]. Because the elderly are more vulnerable to drug-induced AKI and usually have poor renal recovery [14,15], AKI during anti-TB treatment may be more common and serious in Taiwan, where more than 50% of TB patients are older than 65 years. Furthermore, prognostic factors have never been investigated. "
    [Show abstract] [Hide abstract] ABSTRACT: Patients on anti-tuberculosis treatment may develop acute kidney injury (AKI), but little is known about the renal outcome and prognostic factors, especially in an aging population. This study aimed to calculate the incidence of AKI due to anti-TB drugs and analyze the outcomes and predictors of renal recovery. From 2006 to 2010, patients on anti-TB treatment were identified and their medical records reviewed. Acute kidney injury was defined according to the criteria established by the AKI Network, while renal recovery was defined as a return of serum creatinine to baseline. Predictors of renal recovery were identified by Cox regression analysis. Ninety-nine out of 1394 (7.1%) patients on anti-TB treatment had AKI. Their median age was 68 years and there was male predominance. Sixty (61%) developed AKI within two months of anti-TB treatment, including 11 (11%) with a prior history of rifampin exposure. Thirty (30%) had co-morbid chronic kidney disease or end-stage renal disease. The median time of renal recovery was 39.6 days (range, 1-180 days). Factors predicting renal recovery were the presence of fever, rash, and gastro-intestinal disturbance at the onset of AKI. Sixty-two of the 71 (87%) patients who recovered from AKI had successful re-introduction or continuation of rifampin. Renal function impairment is not a rare complication during anti-TB treatment in an elderly population. The presence of fever and rash may be associated with renal recovery. Rifampin can still be used in most patients who recover from AKI.
    Full-text · Article · Jan 2014 · BMC Infectious Diseases
  • [Show abstract] [Hide abstract] ABSTRACT: Acute Interstitial nephritis is an inflammatory parenchymal renal disease with major involvement of the tubules and interstitial regions of the kidney. It encompasses many etiologies including idiopathic disease, and forms associated with the use of medications, infectious agents, and autoimmune disorders. Although the mechanisms of renal damage may vary from one etiology to another, cellular interstitial infiltrates and “tubulitis” are hallmarks of the disease process. Clinical features also vary, but most patients present with acute kidney injury which is often non-oliguric in nature. In many medication-related forms the clinical picture is characterized by rash, fever, and eosinophilia, while the urinary findings are of hematuria and eosinophiluria. Therapy must be directed at the underlying etiology of the disease process, but use of steroids and perhaps other immunosuppressives appear to be of value in some patients.
    No preview · Chapter · Jan 2014
  • [Show abstract] [Hide abstract] ABSTRACT: Measurement of retinol-binding protein 4 in urine (uRBP4) is arguably the most sensitive biomarker for loss of function of the human proximal renal tubule. Megalin- and cubilin-receptor-mediated endocytosis normally absorbs > 99% of the approximately 1.5 g/24 h of protein filtered by the renal glomerulus. When this fails there is “tubular proteinuria,” comprising uRBP4, albumin, and many other proteins and peptides. This tubular proteinuria is a consistent feature of the renal Fanconi syndrome (FS) and measurement of uRBP4 appears to be an excellent screening test for FS.
    No preview · Chapter · Dec 2014
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