Corrección de la anemia en hemodiálisis, efecto del fierro intravenoso sin eritropoyetina / Correction of anemia in hemodialysis, effect of intravenous iron without erythropoietin

BACKGROUND: In the last two decades, the use of erythropoietin for the correction of anemia in hemodialysis patients has been recommended. In Chile, only 10 per cent of hemodialysis patients use erythropoietin, therefore, the correction of iron deficiency must be optimized. AIM: To report the effects of intravenous iron without erythropoietin in the management of anemia in hemodialysis patients. MATERIAL AND METHODS: Retrospective analysis of 42 patients that received intravenous ferrous sacharate in doses of 100 mg/week during 5 weeks and 100 mg bimonthly during six months. These patients did not receive erythropoietin. RESULTS: Thirty six patients had iron deficiency. Basal ferritin was 137 +/- 22 micrograms/l and increased to 321 +/- 28 micrograms/l after treatment. Packed red cell volume increased from 24 +/- 2 per cent to 29 +/- 3 per cent. No adverse effects were reported. CONCLUSIONS: Iron deficiency is frequent in hemodialyzed patients. Intraveineous iron is safe and effective in the treatment of iron deficiency in these patients.

[Renal scleroderma crisis. Role of scleroderma vasculopathy in the induction of cutaneous and visceral fibrosis in 2 cases]. / Crisis de esclerodermia renal. Rol de la vasculopatía esclerodérmica en la inducción de fibrosis cutáneo-visceral en dos casos.

Although fibrosis and vasculopathy coexist in most patients with progressive systemic sclerosis, it is not clear if these events are the result of an unique etiologic factor or if one is consequence of the other. We report two cases of progressive systemic sclerosis that evolved to a renal scleroderma crisis. A 36 years old female presented with a Sjögren syndrome and painful subcutaneous nodules whose biopsy showed perivascular lymphocytic infiltration, perivascular thickening and normal skin. The ESR was 100 mm/h. She developed an hypertensive crisis and progressive renal failure, followed by a rapidly evolving progressive systemic sclerosis. The patient died in the course of this crisis. A 32 years old female with a progressive systemic sclerosis refractory to D-penicillamine treatment, receiving cyclosporin, presented a renal scleroderma crisis, that was successfully treated, with complete recovery of renal function. We highlight the different evolution of these cases, probably due to an early diagnosis and a better experience in the management of this condition.

[Decompensated diabetes mellitus and hyperchloremic metabolic acidosis: a case with both pathologies]. / Diabetes mellitus descompensada y acidosis metabólica hiperclorémica: asociación de patologías en un caso.

Diabetic ketoacidosis is manifested by elevated blood glucose levels, ketosis and metabolic acidosis with increased anion gap. A transitory hyperchloremic acidosis, with normal anion gap, can appear. We report a 21 years old female with a type 2 diabetes mellitus, admitted to the emergency room of a general hospital with hyperglycemia, absence of ketonemia, severe hypokalemia and hyperchloremic metabolic acidosis. Initially, she was diagnosed and treated as a severe diabetic ketoacidosis. Normal blood glucose levels were rapidly achieved but electrolyte and acid base alterations persisted, leading to the suspicion that another associated condition was causing the acidosis and hypokalemia. Urinary pH and anion gap measurement, the study of renal acidification and a bicarbonate overload test lead to the diagnosis of a distal renal tubular acidosis, secondary to a Sjögren syndrome, that was confirmed with a Schirmer test and positive anti Ro antibodies. In this diabetic patient, the acute hyperglycemia intensified the hypokalemia of her distal renal tubular acidosis and unchained the acute metabolic condition.

[Comparison of extra renal potassium management in hypertensive, diabetic and normal subjects]. / Estudio comparativo del manejo extrarrenal de potasio en sujetos controles, pacientes hipertensos y diabéticos.

BACKGROUND: Sodium and potassium ions are involved in the regulation of blood pressure and the genesis of hypertension. AIM: To assess internal potassium balance, as a measure of sodium pump activity, in subjects with essential hypertension and diabetic patients. PATIENTS AND METHODS: Eleven hypertensive subjects, 5 non-insulin-dependent diabetics and 16 age matched controls were studied. An acute oral load of 0.8 mEq/Kg body weight of KCl was administered and blood samples were drawn every 30 min thereafter, until 120 min, to measure plasma K+ levels. Urinary K+ excretion during this period was also measured. In eight hypertensive patients, the test was repeated after two week of supplementation with 60 mEq/day of KCl. The maximal increase in plasma potassium levels and the time required to achieve the maximum concentration was recorded. RESULTS: All patients had normal serum creatinine levels. Mean fasting blood glucose of diabetic patients was 133 +/- 15.1 mg/dl. No difference between patients and controls in maximal increase plasma potassium increase, was observed. In hypertensive patients the lapse to achieve the maximal potassium concentration was longer than in controls. After the period of potassium supplementation in hypertensive patients, there was a significant increase in basal plasma K+ levels and the temporal pattern of plasma potassium increase was similar to that of controls. Between 63 and 68% of retained K+ load was translocated to the intracellular space at 120 min in all study groups. CONCLUSIONS: Internal potassium balance is not significantly altered in subjects with essential hypertension or in non-insulin-dependent diabetics.

[Hepatic veno-occlusive disease associated to the use of azathioprine in a renal transplant recipient]. / Enfermedad venooclusiva hepática asociada a terapia con azatioprina en un paciente trasplantado renal.

We report a 30 years old male, recipient of a kidney allograft and treated with azathioprine, who eighteen days after transplantation had a clinically asymptomatic elevation of total bilirubin and alkaline phosphatases. Nineteen months later, he presented with mild ascites, with a total bilirubin of 3.5 mg/dl, alkaline phosphatases of 308 U/L (normal < 170 U/L) and a prothrombin time at 55% of control. A liver biopsy showed sinusoidal and perivenular fibrosis without inflammation, compatible with chronic venous obstruction. Hepatic veno-occlusive disease is an infrequent complication of azathioprine use.

Tissue-specific modulation of Na, K-ATPase alpha-subunit gene expression in uremic rats.

Chronic renal failure in the rat is associated with an impaired extrarenal potassium handling, whereas a renal adaptive mechanism of the remaining nephrons has been described. To understand the molecular basis of potassium homeostasis during renal failure we investigated the in vitro pump activity and the catalytic mRNA transcription in three different tissues: skeletal muscle, isolated adipocytes and kidney. The activity of the sodium pump, as measured by ouabain-sensitive 86Rb/K uptake in isolated adipocytes and skeletal muscle fibers, revealed a significant reduction of the pump activity in uremic rats. The reduction of the Na, K-ATPase activity in adipose tissue was associated with a similar decrement of both catalytic subunits (alpha 1 and alpha 2), whereas in the skeletal muscle tissue was only related to a decrease in the activity of the alpha 1 isoform. The expression of rat Na, K-ATPase catalytic isoforms mRNAs in kidney, muscle and adipose tissue from control and chronic renal failure rats was investigated at the molecular level with cDNA probes specific for the catalytic isoforms (alpha 1 and alpha 2). Northern blot analysis revealed that the respective catalytic mRNAs of uremic rats are regulated in a tissue-specific manner that are in agreement with the sodium-potassium pump activity. Muscle and adipose tissue showed a decrement in the levels of expression for the alpha 1 isoform mRNA. In contrast to these tissues, an increment in alpha 1 mRNA expression was observed in the kidney of rats with chronic renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)

[Brief history of nephrology in Chile]. / Breve historia de la nefrologia en Chile.

The development of nephrology in Chile is described. The advances in the study and treatment of acute renal failure, urinary tract infections, hypertension, glomerulopathies and other areas are analyzed. The present state of dialysis and transplantation programs is highlighted and the activities of Pediatric and Internal Medicine nephrology branches are summarized.

Effect of chronic renal failure on Na,K-ATPase alpha 1 and alpha 2 mRNA transcription in rat skeletal muscle.

Previous studies have suggested that an alteration in the expression of the Na,K-ATPase of muscle may be an important determinant of enhanced insulin sensitivity in chronic renal failure. Therefore, in the present studies we have examined the effect of uremia on the Na,K-ATPase alpha isoforms in skeletal muscle, at the level of mRNA expression and enzymatic activity. The activity of the sodium pump, as measured ouabain-sensitive 86Rb/K uptake in soleus muscle, revealed a reduction in the activity in uremia, related to the increment in plasma creatinine values. The decrement in 86Rb uptake by the rat soleus muscle of experimental animals was associated with changes on Na,K-ATPase gene product. Northern analysis of mRNA revealed isoform-specific regulation of Na,K-ATPase by uremia in skeletal muscle: a decrease of approximately 50% in alpha 1 subunit Na,K-ATPase mRNA, as compared to controls. The decrement in alpha 1 mRNA correlates with the decreased activity of the Na,K-ATPase in uremia, under basal conditions and with the almost complete inhibition of the Na,K-ATPase, of uremic tissue by a concentration of 10(-5) M ouabain. Although the activity of the alpha 2 isoform pump was not modified by uremia, the 3.4-kb message for this enzyme was increased 2.2-fold; this discrepancy is discussed. Altogether these findings demonstrate that the defective extrarenal potassium handling in uremia is at least dependent in the expression of alpha 1 subunit of the Na,K-ATPase.

[Emphysematous pyelonephritis: 3 cases]. / Pielonefritis enfisematosa: 3 casos.

We report 3 patients who developed emphysematous pyelonephritis. All were diabetic females over 50 years of age with unilateral necrotizing pyelonephritis. Intra and perirenal gas was demonstrated and all patients had infection by E coli. X ray and ultrasound studies allowed the diagnosis. Antibiotic therapy was unsuccessful and all patients had to be operated on.

Enhanced insulin sensitivity in extrarenal potassium handling in uremic rats.

Translocation of potassium to the intracellular compartment is impaired in advanced chronic renal failure. The purpose of this study was to evaluate the role of endogenous insulin in the disposal of an oral potassium load in uremia. Experiments were done on male Sprague-Dawley rats. Chronic renal failure (CRF) was induced by 3/4 nephrectomy. The results show that the addition of oral glucose to a potassium load was more effective in the translocation of potassium to the intracellular compartment in uremic animals. Further, suppression of endogenous insulin secretion with somatostatin caused a much higher increase in plasma potassium (K) of uremic rats (1.09 +/- 0.15 mEq/liter in CRF vs. 0.28 +/- 0.03 mEq/liter in control). Experiments to assess the activity of the Na pump were done in soleus muscles derived from these animals. Although a 50% reduction of the basal Na pump activity was found in the uremic muscles, the addition of insulin 100 mU/ml caused a relatively greater stimulation of ouabain-sensitive 86Rb uptake in the uremic muscle as compared to the control tissue (203% vs. 77% increment). These data suggest a greater sensitivity to insulin action on extrarenal potassium disposal in uremia.

[Enalapril in essential arterial hypertension]. / Enalapril en hipertension arterial esencial.

The hypotensive effect of enalapril, a converting enzyme inhibitor, given as a single agent once daily, was evaluated prospectively over a 16 week period in 20 subjects. One patient abandoned therapy and 2 were withdrawn (increased creatinine levels in one and the need for associated therapy in the other). Side effects developed in 3 patients: creatinine elevation, skin rush and a "salty taste", respectively. A significant decrease in blood pressure (p less than 0.01) attaining normal levels in 6 out of 17 patients was observed. Normal blood pressure levels were not reached in severe hypertension; the association of hydrochlorothyazide was effective in 5 of 11 such subjects. Thus, enalapril may be safely used as a first stage single therapy in mild or moderate hypertension.

Effect of a simultaneous potassium and carbohydrate load on extrarenal K homeostasis in end-stage renal failure.

Patients with chronic renal failure (CRF) are continuously exposed to hyperkalemia. In these patients the extrarenal disposal of a potassium load may be very important to determine the plasma potassium levels. We studied the effect of a combined oral load of potassium (0.5 mEq/kg body weight) and carbohydrate (0.5 g/kg body weight) to mimic normal ingestion of potassium. Eight CRF patients and 5 control subjects were studied. The maximal increase in plasma potassium levels achieved was significantly higher in the patients (1.07 +/- 0.1 mEq/l) than in controls (0.39 +/- 0.05 mEq/l). Basal insulin levels were higher in the CRF patients and increased with the oral potassium and carbohydrate load in both controls and patients. In the CRF patients only 58.9 +/- 3% of the potassium load was translocated to the intracellular space compared to 81 +/- 6% in the controls. No correlation was found between the acid base status and maximal potassium increase. We conclude that patients with CRF exhibit an impaired extrarenal handling of potassium and that this abnormality does not appear to be related to insulin secretion or acid base status.

Alpha 2-agonists block ADH action in toad bladder and this inhibition is not modified by indomethacin.

To identify the type of alpha-adrenoceptors involved in the inhibition of the hydrosmotic effect of antidiuretic hormone (ADH) on the toad bladder, we studied the effect of different alpha-adrenergic agonists and antagonists on ADH-induced water transport. Serosal addition of epinephrine (10(-6) M) and norepinephrine (10(-6) M) in the presence of 10(-4) M propranolol significantly inhibited the hydrosmotic effect of ADH (arginine vasopressin). This inhibitory effect of the catecholamines was completely reversed by 10(-5) M yohimbine but not by prazosin. Clonidine did not block ADH-induced water transport, but guanabenz, another alpha 2-agonist, inhibited water transport in response to ADH. In bladders pretreated with indomethacin to block prostaglandin synthesis, basal water permeability was increased, and even in this condition epinephrine inhibited ADH-induced water transport. These studies indicate that alpha 2-adrenergic receptors are involved in the inhibitory effect of catecholamines on ADH-mediated water permeability in the toad bladder. However, this effect was not mimicked by clonidine, as in the case of rabbit cortical collecting tubule. The inhibitory effect of epinephrine appears to be exerted independently of prostaglandin synthesis.

Lack of potassium effect on Na-Cl cotransport in the medullary thick ascending limb.

The effect of potassium on sodium chloride uptake into rabbit renal medullary thick ascending limb of Henle's loop (mTALH) cells was studied to assess whether K participates in the Na-Cl cotransport system. Na uptake into the mTALH cells was inhibited 70% at 3 min by 1 mM furosemide. The total and furosemide-sensitive Na uptake was stimulated by Cl. Additionally, Cl uptake into the mTALH cells was stimulated by Na gradients and inhibited 42% at 3 min by 1 mM furosemide. Na uptake was studied in the presence of 0,5, or 140 mM external K gradients. Na uptake was similar in the absence and presence of K. Additionally, furosemide inhibited Na uptake as effectively in the absence or presence of K. Similar studies were conducted to study the effects of Na on 86Rb uptake. Na did not stimulate 86Rb uptake. The uptake of 86Rb was similar in the presence of 0,5, or 140 mM Na gradients. Furosemide had no significant inhibitory effect on 86Rb uptake. Barium (5 mM), an inhibitor of K conductance pathways, inhibited total 86Rb uptake by 19%. In the presence of 5 mM BaCl2, Na still did not have a stimulatory effect on 86Rb uptake. The results confirm the existence of a Na-Cl cotransport system in mTALH cells, but a direct effect of K on the NaCl cotransport system could not be demonstrated under the experimental conditions we used.

Hyperkalemia.

These discussions are selected from the weekly staff conferences in the Department of Medicine, University of California, San Francisco. Taken from transcriptions, they are prepared by Drs Homer A. Boushey, Associate Professor of Medicine, and David G. Warnock, Associate Professor of Medicine, under the direction of Dr Lloyd H. Smith, Jr, Professor of Medicine and Chairman of the Department of Medicine. Requests for reprints should be sent to the Department of Medicine, University of California, San Francisco, School of Medicine, San Francisco, CA 94143