A clinical study of renal tubular dysfunction in Cleistanthus collinus (Oduvanthalai) poisoning

Abstract

Introduction. Self-poisoning through the ingestion of Oduvanthalai is common in South India. Mortality may occur because of arrhythmias, renal failure, shock, and respiratory distress. The mechanisms of toxicity are unclear. This prospective, clinical study was designed to assess renal tubular dysfunction because of Oduvanthalai poisoning. Methods. Thirty-two consecutive patients admitted with Oduvanthalai poisoning at a tertiary care hospital in South India, from June 2007 to August 2009 (26 months), were evaluated through history, physical examination, and laboratory studies. Following an interim analysis, additional studies of renal tubular function were performed on a subcohort of eight patients. These included the following: () urinary pH, daily serum, and urine anion gap; () 24-h urine protein and potassium; and () assessment of urine hexosaminidase and amino acid levels. Results. Metabolic acidosis (100%), which persisted at discharge (65.6%), hypokalemia (62.5%), and renal failure (15.6%), was apparent in the total cohort. Tests of renal tubular function on the subcohort revealed a normal anion gap, hyperchloremic, metabolic acidosis of renal etiology, defective urinary acidification, and hypokalemia with kaliuresis, indicative of distal renal tubular acidosis in six patients. Urinary hexosaminidase and amino acid levels, markers of proximal tubular dysfunction, were elevated in seven and two patients, respectively. Conclusions. Distal renal tubular acidosis is an important feature of Oduvanthalai poisoning. Proximal tubular injury and, in more severe forms, global tubular dysfunction with diminished glomerular filtration rate may occur.

Keywords:

• Distal renal tubular acidosis
• Cleistanthus collinus
• Hypokalemia
• Metabolic acidosis
• Hexosaminidase

Acknowledgments

This work was supported by the South Asian Clinical Toxicology Research Collaboration (SACTRC) funded by Wellcome Trust and National Health and Medical Research Council International Collaborative Research Grant 071669MA along with the Australian National University that included a research fellowship to Keshavan Nampoothiri and Anisa Begum. We acknowledge the Neurochemistry Laboratory, Department of Neurological Sciences, Christian Medical College, Vellore, for the assay of urinary amino acids and hexosaminidase A and B.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this paper.