Rafael Díaz-Tejeiro

Loss of renal graft due to recurrent IgA nephropathy with rapidly progressive course: an unusual clinical evolution.

Recurrence of IgA nephropathy following renal transplantation has been described in 40-50% of patients, and it usually has a good outcome. We present the case of a 54-year-old man with IgA nephropathy who developed terminal renal failure in 1985, 3 years after the onset of the disease. In March 1986 he received a cadaveric renal allograft following treatment with ciclosporin and steroids. Eight months later he developed microhaematuria and proteinuria and 10 months later he developed acute nephritic syndrome and rapidly progressive renal failure. Renal biopsy disclosed an IgA nephropathy with epithelial crescents in 60% of glomeruli. Treatment with plasma exchange and cyclophosphamide was unsuccessful and the patient lost his graft and returned to regular haemodialysis 15 months after renal transplantation.

IRREVERSIBLE ACUTE RENAL FAILURE AFTER EXTRACORPOREAL SHOCK-WAVE LITHOTRIPSY

Rafael Díaz-Tejeiro, Department of Nephrology, Hospital Virgen de la Salud, E-45004 Toledo (Spain) Dear Sir, Extracorporeal shock-wave lithotripsy (ESWL) was introduced clinically in February 1980 by Chaussy et al. [1], and it has been in clinical use for 11 years having replaced other treatment techniques for the majority of surgical calculi in the upper urinary tract. Since that time, approximately 2 million patients around the world have been successfully treated by this technique. Patient acceptance and clinical adoption of ESWL has been facilitated by the perception that ESLW does not cause severe acute or lasting side effects [2]. Most complications are related to obstruction from stone fragments lodged within the ureter with accompanying colic and/or infection and subcapsular or perire-nal hematoma [3]. We report the case of a patient with a single functioning kidney who was treated with ESLW developing irreversible acute renal failure. A 54-year-old woman was admitted to the hospital with severe renal failure (Cr = 751 μmol/l; 8.5 mg/dl). Diagnostic evaluation with ultrasound scan revealed bilateral obstructive staghorn calculi. Nephrostomy was performed in the left kidney because the right kidney showed no renal cortex. Renal function recovered to a Cr value of 132 μmol/l (1.5 mg/dl), and pyelolithotomy was performed. Two months later, ESWL was initiated to treat the remaining calculi. A total of 5,000 shock waves with the clinical power setting of 10 (on the scale of 1-10) was administered with the Wolf Piezolith 2500 lithotriptor. No ureteral stents were used. Following monitoring in the recovery room for 2 h, the patient was discharged from the hospital with the prescription of ciprofloxacin orally twice a day for 10 days. Six hours after postoperative procedure, she developed gross hematuria for 2 days. Two days later chemistry studies showed a rise in serum Cr to 398 μmol/l (4.5 mg/dl). Physical examination was normal. Blood pressure and body temperature were always in the normal range. Scan ultrasound revealed loss of corticomedullary demarcation and hypoecogenic parenchyma. Slight

Red cell distribution width: a method that improves detection of iron deficiency in chronic hemodialysis patients.

Rafael Díaz-Tejeiro, MD, Department of Nephrology, University Clinic, School of Medicine, University of Navarra, E-31080 Pamplona (Spain) Dear Sir, The pathogenesis of anemia of maintenance hemodialysis patients is multifactorial. Superimposed iron deficiency because of the repetitive blood losses associated with dialyzer use and bleeding secondary to uremic gastroenteritis and platelet dysfunction is a common feature [1]· The sensitivity of various iron measurements varies with the severity of iron lack. On this basis iron deficiency is commonly divided into three stages: storage iron depletion, iron-deficient erythropoiesis and iron deficiency anemia [2]. Red cell indices, such as mean corpuscular volumen (MCV), mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration, are sensitive only in the second and the third stages [2]. Moreover, several reports have shown that the serum iron and trans-ferrin saturation are of little value in identifying iron deficiency in these patients [3]. Serial measurements of serum ferritin levels provide an acceptable alternative for monitoring iron balance in chronic hemodialysis patients [4]. The majority of studies have suggested that iron deficiency is associated with serum ferritin values of less than 55 ng/dl [5]. The use of a new red blood cell parameter, the red blood cell distribution width (RDW), which is offered as a routine parameter on automated blood count, in combination with MCV improves the classification of anemias and the early detection of iron deficiency [6, 7]. It has been demonstrated that RDW values greater than 14.6% are associated with decreased iron stores [6]. To evaluate the usefulness of the RDW in detecting iron deficiency we examinated blood samples from 27 patients in maintenance hemodialysis. Patients with morphologically identified red cell abnormalities and patients with MCV values greater than 100 fl were excluded because these abnormalities may also cause RDW elevation. All patients were treated with phosphate binders Table 1. Relation of MCV and MC V/ RDW with serum ferritin in 27 patients in chronic hemodialysis

Effects of Xipamide on Transmembranary Potassium Movements and Prostacyclin Production

Several observations suggest a possible interaction between ion transport mechanisms and the arachidonic acid cascade in the natriuretic and in the antihypertensive effects of diuretics(1). Moreover, several studies have established that some diuretic drugs may act on the arachidonic acid cascade(2). In fact, it has been recently reported that the modification of K+ transmembrane gradient by some diuretic drugs may stimulate the generation of prostacyclin, PGI2,(3), Xipamide, X, is a sulfonamide type drug with diuretic and antihypertensive effects but whose mechanism of action remains unknown(4). We, thus, have investigated whether X does modify transmembranary K+ movements and PGI2 production.