[Polycystic kidneys in adults. A clinical study of 106 cases (author's transl)]. / Riñones poliquístics del adulto. Estudio clínico de 106 casos.

A series of 106 cases of polycystic kidneys in adults is presented. The main clinical, exploratory and therapeutic data are analyzed. The average age of the patients at the time of the first clinical manifestation was 35 years; average age at the time of diagnosis was 43 years. The most common forms of presentation included renal colics, blood hypertension, noncolic lumbar pain, macroscopic hematuria, and polydipsia-polyuria. The most frequent symptoms were: abdominal pain of any type (73 patients), polydipsia-polyuria (66 patients), blood hypertension (61 patients), macroscopic hematuria (47 cases), episodes of urinary infection (41 cases), and passing of calculi (22 cases). Seventy-eight subjects had arterial high blood pressure; it was easily controlled in all except 14 cases. Proteinuria was slight in all except two cases. Values for hematocrit and hemoglobin remained high in relation to the degree of renal insufficiency. The mean value of hematocrit in patients with creatinine clearance below 10 ml/min was 30 percent. Renal function decreased gradually, from normal to a clearance of less than 10 ml/min over a period of 12 years on the average. Diagnosis was based mainly on abdominal physical examination and intravenous urography; 89 patients had palpable abdominal masses. Urography revealed typical images of polycystic kidney in every case. The following associated conditions were also discovered: liver cysts (17 cases among 57 liver scanning; bilateral ovarian cysts in one case; Cacci-Ricci's disease in one case; and cerebral arterial aneurysms in another patient. Treatment was conservative with the aim to control arterial blood pressure and urinary infection. Twenty-nine patients required saline replacement; peritoneal dialysis was practiced in two cases and permanent hemodialysis was prescribed for 15 individuals.

[Vascular approach for periodic hemodialysis. Clinical course of 100 internal arteriovenous fistulas (author's transl)]. / Acceso vascular para hemodiálisis periódicas. Evolución de 100 fístulas arteriovenosas internas.

The clinical course of 100 internal arteriovenous fistulas in patients observed over a period of more than 6 months was analyzed. Ninety-six were practiced in the upper extremities as side-to-side anastomoses in the forearm between the radial artery and the nearest vein; three were constructed in the lower limbs as anastomoses between the femoral artery and the internal saphenous vein; and one was an autograft of the saphenous vein in the forearm. The most important complications observed were thrombosis (arising chiefly from scant venous development, surgical procedures, and episodes of arterial hypotension), distal ischemia, distal venous flow, infection of the fistula, and insufficient flow. A blood flow over 350 ml/min was achieved in all except two patients. The actuarial survival of individuals with arteriovenous fistulas is high at the present time, with 86 percent of the fistulas functioning after 3 years. The longest period of satisfactory arteriovenous fistula function is 8 years and 3 months.

[Nodular regenerative hyperplasia of the liver associated with a CREST syndrome with multiorgan involvement]. / Hiperplasia nodular regenerativa hepática asociada a síndrome CREST con afección multivisceral.

A 52 year old woman with CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal hypomotility and telangiectasia) and visceral involvement of the kidneys, lungs and liver is presented. The hepatic implication was a focal nodular hyperplasia of the liver which is a component not frequently recognized. Another 4 cases of this syndrome, associated to different forms of scleroderma, were described previously. Because of the way in which this case developed, this disease should be suspected when alkaline phosphatase and gamma-glutamyltranspeptidase levels are elevated. We comment on the utility of the laparoscopy and liver biopsy in diagnosing the diseased and the situation found. Finally, we discuss the pathogenic implications of the disease with scleroderma, owing to the vascular mechanism.

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Relación entre obesidad y desarrollo de insuficiencia renal / Relationship between obesity and development of kidney failure

La incidencia de la glomerulopatía asociada a la obesidad está alcanzando proporciones tremendas durante la última década. La lesión más frecuentemente encontrada en las biopsias renales de los pacientes obesos con proteinuria es la glomeruloesclerosis segmentaria y focal. Diversos estudios epidemiológicos han demostrado que la obesidad es un importante factor de riesgo para el desarrollo de proteinuria e insuficiencia renal en la población sana. Los mecanismos por los que la obesidad puede inducir proteinuria son desconocidos, aunque existen evidencias que apuntan hacia la participación de factores hemodinámicos, hiperlipidemia y un aumento de sustancias vasoactivas y fibrogénicas, entre las que se incluyen la angiotensina II, insulina, leptina y el factor transformador de crecimiento beta. La pérdida de peso produce una marcada reducción de los componentes del sistema renina-angiotensina-aldosterona. El aumento del índice de masa corporal es un factor de riesgo para el desarrollo de proteinuria o insuficiencia renal en pacientes con disminución de la masa renal funcionante (uninefrectomizados o agenesia renal). Aunque los inhibidores de la enzima convertidora de la angiotensina han mostrado una acusada influencia favorable sólo temporalmente, la pérdida de peso produce un descenso en la proteinuria en las nefropatías crónicas proteinúricas de cualquier entidad. La prevención y tratamiento de la obesidad debe ser un objetivo primordial dentro de los pacientes diabéticos y no diabéticos con enfermedad renal crónica (AU)

The incidence of obesity-related glomerulopathy has been reaching tremendous proportions over the last decade. The most frequently found lesion in kidney biopsies of obese patients with proteinuria is focal segmental glomerulosclerosis. Different epidemiological studies have demonstrated that obesity is an important risk factor for the development of proteinuria and renal failure in the normal population. The mechanisms by which obesity may induce proteinuria are unknown. However, there is evidence that points towards the participation of hemodynamic, hyperlipidemic factors and an increase of vasoactive and fibrogenic substances, which include angiotensin II, insulin, leptin and growth transforming factor-beta. Weight loss produces a marked reduction of the renin-angiotensin-aldosterone system. Body mass index increase is a risk factor for the development of proteinuria of kidney failure in patients with decreased functioning kidney mass (nephrectomized or renal agenesis). Although the angiotensin converting enzyme inhibitors have demonstrated a striking favorable influence, only temporally, weight loss produces a decrease in proteinuria in chronic proteinuric nephropathies of any disease. Prevention and treatment of obesity should be a primary objective within diabetic and no-diabetic patients with chronic kidney disease (AU)

Anomalias del transporte paracelular y bases genéticas del sindrome de hipomagnesemia, hipercalciuria y nefrocalcinosis / Abnormalities in paracellular transport and genetic bases in the hypomagnesemia, hypercalciuria and nefrocalcinosis syndrome

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