[Peritoneal implants in patients affected by chronic renal failure in hemodialysis programme]. / Implantes peritoneales en pacientes con insuficiencia renal crónica en programa de hemodiálisis.

The presence of peritoneal implants detected by computered axial tomography (CT) is usually related to mesothelial primary neoformative processes or, more frequently to peritoneal metastasis or peritoneal carcinomatosis. Although the higher prevalence of neoplastic processes in the chronic renal failure population, the association of peritoneal implants and constitutional syndrome is not always correlated to peritoneal carcinomatosis. We present the case of two patients with chronic renal failure in hemodialysis programme, with abdominal insidious clinical, constitutional syndrome and similar peritoneal implants seen by CAT: the histologic analysis of peritoneal implants gave the definitive diagnostic of secondary amyloidosis and peritoneal tuberculosis respectively.

Implantes peritoneales en pacientes con insuficiencia renal crónica en programa dehemodiálisis / Peritoneal implants in patients affected by chronic renal failure in hemodialysis programme

La presencia de implantes peritoneales detectados por tomografía axial computerizada(TAC) suele estar asociada a procesos neoformativos primarios del mesotelioo, más frecuentemente, a metástasis peritoneales o carcinomatosis peritoneal.A pesar de la mayor prevalencia de procesos neoplásicos en la poblaciónafecta de insuficiencia renal crónica, la asociación de implantes peritoneales y síndromeconstitucional no siempre se correlaciona con carcinomatosis peritoneal.Presentamos dos pacientes con insuficiencia renal crónica en programa de hemodiálisis,con clínica insidiosa abdominal, síndrome constitucional e implantesperitoneales de similares características visualizados por TAC. El análisis histológicode los implantes peritoneales permitió el diagnóstico definitivo de amiloidosissecundaria y tuberculosis peritoneal respectivamente

The presence of peritoneal implants detected by computered axial tomography(CT) is usually related to mesothelial primary neoformative processes or, more frequentlyto peritoneal metastasis or peritoneal carcinomatosis. Although the higherprevalence of neoplastic processes in the chronic renal failure population, the associationof peritoneal implants and constitutional syndrome is not always correlatedto peritoneal carcinomatosis. We present the case of two patients with chronicrenal failure in hemodialysis programme, with abdominal insidious clinical,constitutional syndrome and similar peritoneal implants seen by CAT: the histologicanalysis of peritoneal implants gave the definitive diagnostic of secondary amyloidosisand peritoneal tuberculosis respectively

Fracaso renal agudo como forma de presentación clínica de linfoma de Burkitt renal en un paciente HIV positivo / Burkitt’s lymphoma in an hiv positive patient presenting with acute renal failure

El linfoma de Burkitt es un tumor frecuentemente asociado a situaciones de inmunodepresión como puede ser leucemia aguda linfoblástica (L3) o infecciones por el virus de la inmunodeficiencia humana (VIH). La incidencia de la afectación renal es variable (34-62%), respondiendo a diferentes etiologías. Presentamos un caso de fracaso renal agudo en un paciente con linfoma de Burkitt con infiltración renal e infectado por el virus de la inmunodeficiencia humana (AU)

Burkitt’s lymphoma is a tumour often associated with low immunity as acutelymphoblastic leukaemia (l3) or infection by the human immunodeficiency virus(HIV). The incidence of renal affection is variable (34-62%) and there are different aetiologies. We present a case of acute renal failure in a patient with a Burkitt’s lymphoma and renal infiltration, and infected by the human immunodeficiency virus (AU)

[Acute kidney failure as the clinical presenting form of renal Burkitt's lymphoma in an HIV-positive patient]. / Fracaso renal agudo como forma de presentación clínica de linfoma de Burkitt renal en un paciente HIV positivo.

Burkitt's lymphoma is a tumour often associated with low immunity as acute lymphoblastic leukaemia (l3) or infection by the human immunodeficiency virus (HIV). The incidence of renal affection is variable (34-62%) and there are different aetiologies. We present a case of acute renal failure in a patient with a Burkitt's lymphoma and renal infiltration, and infected by the human immunodeficiency virus.

Hypertension and nephrotoxicity in the rate of decline in kidney function in diabetic nephropathy.

Serum creatinine levels were determined prospectively every 2 to 3 months in 40 patients with diabetic nephropathy for a global observation period of 864 months. The monthly creatinine increasing rate was significantly lower in normotensive periods, mean arterial pressure (MAP) less than 115 mmHg, when compared with hypertensive periods, MAP greater than 125 mmHg. No significant difference was shown in periods with borderline hypertension (MAP between 115-124 mmHg). The mean creatinine increases were of 0.036 mg/dl/month, 0.3 mg/dl/month and 0.046 mg/dl/month respectively. Normotension was associated with a slowing down of the rate of decline in renal function in this group of moderate kidney failure with an initial mean serum creatinine of 2.26 mg/dl. The exposure of patients to nephrotoxics (aminoglycosides, and possibly anesthesia) significantly accelerated the decline in renal function: 0.39 mg/dl/month and 0.17 mg/dl/month respectively according to the concomitance or not of toxics and hypertension. The reported protective effect of diabetes against aminoglycosides nephrotoxicity in experimental conditions was not reflected in our clinical results. On the contrary, we suggest a possible enhanced sensibility of the diabetic patient with diabetic nephropathy to aminoglycosides leading to an acceleration of the progression of renal failure.

Relative hyperphosphaturia in diabetic chronic renal failure: a protective factor of hyperparathyroidism.

Relative low serum levels of parathormone (PTH) and low incidence of secondary hyperparathyroidism have been reported in diabetic uremic patients. The pathogenesis of this reported resistance to uremic secondary hyperparathyroidism in diabetes remains controversial. We have measured the serum C-terminal parathormone (C-PTH) renal phosphorus threshold (TmPO4) and nephrogenous cyclic AMP (N-cCAMP), in 2-hour urine collection in 22 patients with diabetic nephropathy with moderate chronic renal failure and in 27 controls with similar creatinine clearance values (18.16 +/- 9.14 and and 19.1 +/- 8.47 ml/min). In spite of the lower levels of serum C-PTH (1.07 +/- 0.43 ng/ml) diabetic patients exhibited an increased phosphaturia (TmPO4: 1.97 +/- 0.9 mg/100 ml GFR) when compared with the control group (C-PTH: 2.01 +/- 1.17 mg/ml, and TmPO4: 2.5 +/- 0.7 ml GFR). When the C-PTH values were plotted against the logarithm of creatinine clearance values, both groups showed a significant linear relationship reflecting the progressive increase in PTH when GFR fell. This progressive parathyroid stimulus was also present in diabetic patients but in a lower intensity. We believe that increased phosphaturia in diabetics with moderate chronic renal failure may be a major factor in precluding the appearance of secondary hyperparathyroidism in these patients once they reach the dialysis and transplantation programs.