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chancer

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Hello,

Wondering if anyone can help me here...Q...how does renal failure or chronic Glomerulonephritis contribute to hypertension? I understand how hypertension can damage blood vessels, but how does a bad kidney contribute to heart damage or Hypertension?

Thanks!
 

just one

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Hypertension is high blood pressure, kidneys can regulate blood pressure by reabsorption of water via Na+ reabsorption. More water = higher blood pressure.

Just off top of my head, sure someone will elaborate more precisely before thread is closed for homework help.
 
Oct 31, 2009
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A quick google search gets this from up to date:

PATHOGENESIS
Hypertension is a frequent finding in both acute and chronic kidney disease, particularly with glomerular or vascular disorders [1]. However, the incidence of hypertension and its pathogenesis vary with the type of renal disease and its duration.
Acute glomerular disease — Patients with acute glomerular disease, such as poststreptococcal glomerulonephritis or membranous nephropathy, tend to be volume expanded and edematous due to sodium retention [2]. As a result, the elevation in blood pressure is primarily due to fluid overload, leading to suppression of the renin-angiotensin system and enhanced release of atrial natriuretic peptide [3]. Although these changes are most prominent with advanced disease, the incidence of hypertension is increased even in patients with a normal serum creatinine concentration [4]. Both a familial predisposition to hypertension and subclinical volume expansion are thought to be important in this setting.
Experimental studies of the nephrotic syndrome or glomerulonephritis suggest that sodium retention in these disorders is due to increased reabsorption in the collecting tubules [5], which is also the site of action of atrial natriuretic peptide and the related renal hormone urodilatin. (See "Natriuretic hormones: Atrial peptides and ouabain-like hormone".)
Two different abnormalities in collecting tubule function have been identified in glomerular disease, both of which could increase sodium reabsorption:

  • Relative resistance to atrial natriuretic peptide, due at least in part to more rapid degradation of the second messenger cyclic GMP (guanosine monophosphate) by the enzyme phosphodiesterase [4]. Infusion of a phosphodiesterase inhibitor largely reverses this defect and restores the normal natriuretic response to volume expansion.
  • Increased activity of the Na-K-ATPase pump in the cortical collecting tubule but not other nephron segments [6]. This pump provides the energy for active sodium transport by pumping reabsorbed sodium out the cell into the peritubular capillary.
 
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Its really a cause & effect ... they both cause each other in other words.

Hypertension will eventually lead to a defect in the renin-angiotensin-aldosterone system. This system failure will result in constant increases in peripheral resistance and elevations in renal salt retention. Excess fluid retention will then continue to exacerbate the problem with hypertension.

If one were to consider the chicken or the egg in this situation, I think it more probable that renal failure causes hypertension more often than vice versa.
 

Myuu

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