¿Los quistes renales simples son otra forma de manifestación de prelitiasis en la infancia?

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Abstract

Los quistes renales simples son lesiones poco frecuentes en pacientes pediátricos. En ausencia de hipopotasemia o de un incremento en la producción de NH4+, se desconoce el origen de los mismos. Hepler, en 1930, propuso que su causa podría ser una obstrucción tubular. Hemos estudiado de forma prospectiva la presencia de hipercalciuria o de hipocitraturia, así como los antecedentes familiares de litiasis en un grupo de niños diagnosticados ecográficamente de quistes renales simples. Al diagnóstico, la edad media de los 22 pacientes (12 varones y 10 mujeres) fue de 6,04 ± 2,9 años. El estudio ecográfico se había solicitado por infección de vías urinarias, dolor abdominal, hematuria u otros. Los quistes fueron ligeramente más frecuentes en el lado izquierdo (54,5%). Todos estaban ubicados en el polo renal superior. En 14 pacientes (63,6%) se demostró que eran portadores de hipercalciuria o hipocitraturia (hipercalciurian = 11, 50%). En 13 familias existían antecedentes de litiasis renal. En conjunto, las anomalías metabólicas estudiadas causantes de cálculos en los niños o los antecedentes familiares de litiasis estaban presentes en 19 familias (86,3%). Nuestra hipótesis es que ambas entidades, quistes renales y predisposición genética a padecer cálculos renales, están relacionadas.

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Based on statistical analysis of data in 186 children, a formula was derived which allows accurate estimation of glomerular filtration rate (GFR) from plasma creatinine and body lenght (GFR(ml/min/1.73 sq m) = 0.55 length (cm)/Per (mg/dl). Its application to clearance data in a separate group of 223 children reveals excellent agreement with GFR estimated by the Ccr (r = .935) or Cin (r = .905). This formula should be useful for adjusting dosages of drugs excreted by the kidney and detecting significant changes in renal function.

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Alfredo Torres, Jock W. Young, K Offord … (1990)

The recognition of renal cysts in two patients with chronic hypokalemia and the renal effects of hypokalemia in certain species of animals prompted this study of the possible association of hypokalemia and renal cysts in patients with primary aldosteronism or primary renal potassium wasting. Using CT scans, we studied 55 patients with primary aldosteronism, of whom 24 had cysts (44 percent). The cysts were more frequent in patients with adrenal tumors than in those with idiopathic adrenal hyperplasia. Sixteen of the 26 patients with tumors (62 percent) had renal cysts, which were often multiple and located in the medulla. Lower plasma potassium levels and higher serum aldosterone levels, urinary aldosterone excretion, and plasma renin activity were correlated with the extent of the cystic disease. Sequential observations indicated that prolonged hypokalemia can be accompanied by the development of renal scarring and that the size and number of cysts can decrease markedly in some patients after the removal of an adrenal adenoma. The association of hypokalemia, aldosteronism, and renal cysts was also supported by the finding of multiple medullary cysts in two patients with primary renal potassium wasting. We conclude that chronic hypokalemia is accompanied by enhanced renal cytogenesis and may lead to interstitial scarring and renal insufficiency. Renal cysts are thus dynamic structures whose growth can be influenced by hormonal or pharmacologic interventions.