Related Experiment Video

Updated: Jun 13, 2026

Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions
06:32

Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions

Published on: June 13, 2025

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

Keshavan Nampoothiri1, Anugrah Chrispal, Anisa Begum

  • 1Department of Medicine Unit 1, Christian Medical College, Vellore, Tamil Nadu, India.

Clinical Toxicology (Philadelphia, Pa.)
|April 20, 2010
PubMed
Abstract

Insights

Oduvanthalai poisoning commonly causes distal renal tubular acidosis and hypokalemia in South India. Some patients also experience proximal tubular injury, leading to impaired kidney function.

Area of Science:

  • Toxicology
  • Nephrology
  • Clinical Medicine

Background:

  • Oduvanthalai (Cerbera odollam) self-poisoning is prevalent in South India, often leading to severe complications like arrhythmias, renal failure, shock, and respiratory distress.
  • The precise mechanisms underlying Oduvanthalai toxicity remain incompletely understood.
  • This study aimed to investigate renal tubular dysfunction following Oduvanthalai ingestion.

Purpose of the Study:

  • To assess the prevalence and characteristics of renal tubular dysfunction in patients with Oduvanthalai poisoning.
  • To elucidate the specific types of tubular damage (proximal vs. distal) caused by Oduvanthalai toxicity.
  • To identify key clinical and laboratory markers associated with Oduvanthalai-induced nephrotoxicity.

Main Methods:

  • A prospective clinical study involving 32 patients admitted with Oduvanthalai poisoning over 26 months.
  • Evaluation included patient history, physical examination, and standard laboratory tests.
  • In-depth renal tubular function tests were conducted on a subcohort of eight patients, including urinary pH, serum/urine anion gap, 24-h urine protein and potassium, and urinary hexosaminidase and amino acid levels.

Main Results:

  • All patients (100%) presented with metabolic acidosis, with 65.6% showing persistence at discharge.
  • Hypokalemia (62.5%) and renal failure (15.6%) were significant findings in the cohort.
  • Subcohort analysis revealed distal renal tubular acidosis in six patients, characterized by defective urinary acidification and hypokalemia with kaliuresis. Elevated urinary hexosaminidase and amino acid levels indicated proximal tubular dysfunction in several patients.

Conclusions:

  • Distal renal tubular acidosis is a significant and common complication of Oduvanthalai poisoning.
  • Oduvanthalai ingestion can lead to proximal tubular injury.
  • In severe cases, Oduvanthalai poisoning may result in global tubular dysfunction and reduced glomerular filtration rate.

More Related Videos

Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis04:37

Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis

Published on: April 25, 2025

Inducing Acute Liver Injury in Rats via Carbon Tetrachloride (CCl4) Exposure Through an Orogastric Tube06:12

Inducing Acute Liver Injury in Rats via Carbon Tetrachloride (CCl4) Exposure Through an Orogastric Tube

Published on: April 28, 2020

Related Concept Videos

Renal Tubule and Collecting Duct01:24

Renal Tubule and Collecting Duct

The renal tubule is divided into three parts: the proximal convoluted tubule (PCT), the Loop of Henle (LOH), and the distal convoluted tubule (DCT).
Proximal Convoluted Tubule (PCT):
The PCT is the initial segment of the renal tubule, extending from the Bowman's capsule that encloses the glomerulus. Its convoluted structure and microvilli-lined cells increase the surface area for reabsorption. The PCT reabsorbs glucose, amino acids, sodium, and water from the filtrate, ensuring essential...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
Enhanced Elimination of Poison01:26

Enhanced Elimination of Poison

Poison can be effectively removed from the gastrointestinal (GI) tract through various decontamination procedures.
Antidotes serve a crucial role in counteracting the effects of poison by inhibiting enzymes responsible for producing harmful drug metabolites. In some cases, these toxic metabolites can be neutralized by endogenous cosubstrates, which are maintained at specific concentrations to prevent interaction with cellular macromolecules and subsequent cell death.
Renal excretion is the...
Renal Drug Excretion: Tubular Secretion01:28

Renal Drug Excretion: Tubular Secretion

Active tubular secretion is a robust, energy-demanding process that utilizes carrier systems to transport drugs into renal tubules. The active renal secretion systems include the organic anion transporter (OAT) for weak acids and the organic cation transporter (OCT) for weak bases. Structurally similar drugs can compete for the same transporter, potentially leading to drug accumulation and toxicity. However, this principle can be exploited therapeutically. One example is probenecid (Probalan),...
Toxidromes: Clinical Features01:30

Toxidromes: Clinical Features

Toxidromes are specific patterns of symptoms resulting from toxic substance exposure. They help in the identification and treatment of poisoning. The symptoms of each toxidrome group indicate poisoning by a certain class of chemicals or drugs.1. Sympathomimetic: Stimulates the sympathetic nervous system. Symptoms include agitation, increased heart rate (HR), blood pressure (BP), respiratory rate (RR), temperature, and pupil size. Drugs like cocaine and amphetamines, along with tremors and...