Causes Of Hypokalemia - Charts

Effect Of Hyperuricaemia On Kidney.

The above picture shows uric acid kidney stone kept in the pathology lab. Let us briefly study the effects of Hyperuricaemia on kidney.

Causes Of Hyperuricaemia: High levels of urate in blood is known as hyperuricaemia. It may result from increased turnover (15%) or reduced excretion of urate (85%)
The causes are given below:

• Drugs: cytotoxics, thiazides, loop diuretics,pyrazinamide
• Increased cell turn over: Lymphoma, leukemia, psoariasisf, hemolysis, muscle death-rhabdomyolysis. 
• Reduced excretion: Promary gout, chronic kidney disease, lead nephropathy, hyper parathyroidism, pre eclampsia
• Others; Hypertension, Hyperlipedaemia 
• Lesch-Nyhan syndrome - a disorder of purine synthesis

Hyperuricaemia and Renal Failure: Severe renal failure from any cause may be associated with hyperuricaemia, and rarely this may cause gout. Sometimes the relationship of cause and effect is reversed so that it is hyperuricaemia that causes the renal failure. This can occur in cytotoxic treatment (tumor lysis syndrome) and in muscle necrosis.

How Urate Causes Renal Failure?
Urate is poorly soluble in water so over excretion can lead to crystal precipitation. Renal failure occurs most commonly becauseurate precipitates in the renal tubules. This may occur at a plasma level > 1.19mmol/L. In some instances uretric obstruction from urate crystals may occur. This responds to retrograde uretric catheterization and lavage.

Autosomal Dominant Polycystic Kidney Disease

A 41-year-old woman with newly diagnosed hypertension reports persistent bilateral flank pain. She gives a family history of “kidney problems.” On urinalysis, she is noted to have microscopic hematuria. An ultrasound and abdominal CT scan show bilateral polycystic kidneys.

Case Discussion:

Poly Cystic Kidney Disease:

Introduction: Polycystic kidney disease (PKD) is a manifestation of a group of inherited disorders resulting in renal cyst development. In the most common form, autosomal-dominant polycystic kidney disease (ADPKD), extensive epithelial-lined cysts develop in the kidney; in some cases, abnormalities also occur in the liver, pancreas, brain, arterial blood vessels, or a combination of these sites. It is the most common tubular disorder of the kidney, affecting 1 in 300 individuals.
It is most frequently seen in the third and fourth decades of life, but can be diagnosed at any age.

Pathophysiology: ADPKD results from mutations in either of 2 genes that encode plasma membrane–spanning polycystin 1 (PKD1) and polycystin 2 (PKD2).2 Polycystins regulate tubular and vascular development in the kidneys and other organs (liver, brain, heart, and pancreas).
PKD1 and PKD2 are colocalized in primary cilia and appear to mediate Ca2+ signaling as a mechanosensor, essential for maintaining the differentiated state of epithelia lining tubules in the kidney and biliary tract. These mutations result in many abnormalities including increased proliferation and apoptosis and loss of differentiation and polarity.