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Related Concept Videos

Nephrotic Syndrome II : Assessment and Medical Management01:26

Nephrotic Syndrome II : Assessment and Medical Management

IntroductionNephrotic syndrome is a kidney disorder marked by excessive protein loss in the urine, leading to various systemic complications. This condition often results from damage to the glomeruli—the kidney's filtering units—causing proteinuria, low blood protein levels, and fluid retention. Understanding the assessment, diagnosis, and management of nephrotic syndrome is essential for effective treatment and prevention of further kidney damage.AssessmentPatient History: Document any history...
Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
Nephrotic Syndrome III : Nursing Management01:24

Nephrotic Syndrome III : Nursing Management

Nursing management for nephrotic syndrome adapts as the disease progresses, with strategies evolving to address advancing symptoms and complications.Early-Stage Management In the early stages, nursing interventions for nephrotic syndrome resemble those used in managing acute glomerulonephritis, focusing on symptom monitoring, fluid balance, and managing mild to moderate edema.Vital Signs: Regularly monitor blood pressure, pulse, respiratory rate, and temperature to promptly identify...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
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).
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Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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Related Experiment Video

Updated: May 11, 2026

A Novel Method: Super-selective Adrenal Venous Sampling
06:08

A Novel Method: Super-selective Adrenal Venous Sampling

Published on: September 15, 2017

Pseudohypoaldosteronism type 1: management issues.

Rajni Sharma1, Meenu Pandey, Sandeep Kumar Kanwal

  • 1Department of Pediatrics, Division of Pediatric Intensive Care, Lady Hardinge Medical College and associated Kalawati Saran Childrens Hospital, New Delhi, India. drrajnisharma@yahoo.com

Indian Pediatrics
|May 18, 2013
PubMed
Summary

A rare genetic disorder, pseudohypoaldosteronism type 1 (PHA1), caused severe salt wasting and hyperkalemia in a newborn. Despite intensive treatment, the infant succumbed to complications, highlighting the critical nature of this condition.

Related Experiment Videos

Last Updated: May 11, 2026

A Novel Method: Super-selective Adrenal Venous Sampling
06:08

A Novel Method: Super-selective Adrenal Venous Sampling

Published on: September 15, 2017

Area of Science:

  • Pediatric Endocrinology
  • Genetics
  • Nephrology

Background:

  • Pseudohypoaldosteronism type 1 (PHA1) is a rare disorder characterized by aldosterone resistance, leading to salt wasting and hyperkalemia.
  • Autosomal recessive PHA1, particularly the multiple target organ dysfunction (MTOD) form, is exceptionally severe and often presents in neonates.

Observation:

  • A newborn female presented with life-threatening hyperkalemia and salt wasting crisis, indicative of severe MTOD PHA1.
  • The infant required aggressive management including intravenous fluids, potassium-lowering agents, sodium chloride supplementation, and peritoneal dialysis.
  • Genetic analysis identified a homozygous mutation in the α-ENaC (epithelial sodium channel) gene.

Findings:

  • The patient experienced a difficult clinical course with persistent hyperkalemia and prolonged hospitalization.
  • Despite medical interventions, the infant's condition did not improve sufficiently.
  • The infant ultimately succumbed to pneumonia and septicemia at four months of age.

Implications:

  • This case represents the first genetically confirmed instance of PHA1 in India.
  • Severe PHA1 poses a significant mortality risk in neonates, emphasizing the need for early diagnosis and management.
  • Understanding the genetic basis of PHA1 is crucial for accurate diagnosis and potential future therapeutic strategies.