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Related Concept Videos

Antihypertensive Drugs: Direct Renin Inhibitors01:25

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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,...
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Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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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...
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Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
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In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
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Updated: Dec 16, 2025

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
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Hydralazine-Induced Isolated Lupus Nephritis.

Naseer Khan1, Ronald Reichel1, Ayesha Khurshid2

  • 1Department of Nephrology, Ochsner Clinic Foundation, Baton Rouge, LA.

Ochsner Journal
|July 3, 2020
PubMed
Summary

Hydralazine can cause drug-induced lupus nephritis, a rare condition affecting only the kidneys. Promptly stopping hydralazine and initiating immunosuppressive therapy led to complete remission in this patient.

Keywords:
Acute kidney injuryhydralazinelupus nephritisnephrotic syndromeproteinuria

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Area of Science:

  • Nephrology
  • Immunology
  • Pharmacology

Background:

  • Hydralazine is an antihypertensive medication with known systemic side effects.
  • Drug-induced lupus erythematosus (DILE) is a recognized adverse effect of certain medications, including hydralazine.
  • Previous reports have linked hydralazine to systemic vasculitis.

Observation:

  • A 79-year-old male with chronic kidney disease developed nephrotic syndrome and acute kidney injury after initiating hydralazine therapy.
  • Kidney biopsy revealed lupus nephritis, and immunologic markers confirmed hydralazine-induced lupus nephritis with positive antihistone antibodies.
  • The patient presented with isolated renal disease, showing no signs of systemic vasculitis.

Findings:

  • Hydralazine therapy precipitated an isolated lupus nephritis presentation.
  • The patient tested positive for antihistone antibodies, a marker associated with drug-induced lupus.
  • Discontinuation of hydralazine and initiation of immunosuppressive therapy resulted in complete remission of lupus nephritis.

Implications:

  • This case highlights the uncommon presentation of isolated renal lupus nephritis induced by hydralazine.
  • Early recognition and management are crucial for favorable outcomes in hydralazine-induced lupus nephritis.
  • The findings underscore the importance of considering drug-induced etiologies in patients presenting with new-onset lupus nephritis.