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The Goodpasture′s syndrome, also konwn as anti-GBM disease, is an uncommon disease, responsible for 20% of all cases of rapidly progressive glomerulonephritis. Anti-GBM antibodies are directed against non-collagenous domain (NC-1) of the alpha-3 chain of type IV collagen. When conventional ELISA assays are used, these antibodies can be detected in almost all the patients. Nevertheless, some reports have described antibody-negative relapsing disease. Some aggravating factors, namely, smoking, pulmonary infection and hypervolemia, may expose embedded antigenic target and may be responsible for the relapse. In addition, these antibody-negative relapses also respond to standard treatment, which comprises of plasma exchange, pulse steroids and cyclophosphamide. Herein, we report a patient who presented at the Selcuk Univer-sity Meram School of Medicine, Meram, Konya, Turkey, with the pulmonary-renal syndrome. He was also found to have idiopathic dilated cardiomyopathy (DCM). To our knowledge, this is the first report describing co-existence of DCM and anti-GBM disease. There is growing evidence showing strong relation of both DCM and anti-GBM disease with HLA. Although not proven, this might have occurred in our patient. In our opinion, volume overload was facilitated by anuria and DCM and led to an antibody-negative pulmonary relapse. The relapse was treated just as the first episode and the patient improved satisfactorily.

Common variable immunodeficiency (CVID) is a heterogenous group of predominantly antibody-deficiency disorders that make up the greatest proportion of patients with symptomatic primary hypogammaglobulinemia. The rare coincidence of amyloidosis and hypogammaglobulinemia has been reported previously. Contrary to the usual insidious, slowly progressive disease following hepatitis C infection, a rapidly progressive cirrhotic form can develop in hypogammaglobulinemic patients. We report a HCV-positive patient with a new onset of nephrotic syndrome and systemic amyloidosis secondary to CVID. Blood analyses showed serum creatinine of 1.8 mg/dL and serum albumin of 3.1 gm/dL; 24-h urinary protein was 11 800 mg/day. Serum immunoglobulin levels were IgG 340 mg/dL, IgM 18 mg/dL, IgA 11 mg/dL. Duodenal biopsy revealed AA-type amyloidosis with potassium permanganate and Congo red staining. After a month of antiproteinuric therapy, the proteinuria was reduced to 3350 mg/day.

Rationale and objectives: Oxidative stress is increased in chronic kidney disease (CKD) patients and end-stage renal disease (ESRD) patients undergoing dialysis treatment. Coenzyme Q10 (CoQ10) is a ubiquitous and strong antioxidant. Role of CoQ10 is not fully evaluated in renal patients. We aimed to investigate the relationship of CoQ10 with oxidant and antioxidant system markers in patients with renal disease. Material and methods: Forty patients with CKD (stages 3--5) who were managed conservatively without dialysis treatment, 40 hemodialysis, and 60 chronic ambulatory peritoneal dialysis (CAPD) patients were included in the study. Biochemical and whole blood analyses were done using hospital auto-analyzers from stored samples. Serum CoQ10, malondialdehyde (MDA), superoxide dismutase (SOD), and antioxidant activity (AOA) levels were determined. Main findings: There was no difference among the groups in terms of serum CoQ10 levels. However, other components of antioxidant system, namely, SOD and AOA were significantly higher in CAPD patients when compared to CKD patients. MDA levels were not significantly different among the groups. Principal conclusion(s): The results of this study showed no difference among CKD, CAPD, and hemodialysis patients in terms of serum CoQ10 levels. [ABSTRACT FROM AUTHOR]

The article presents a case study of a maintenance haemodialysis patient with hypotension and weakness who had undergone cadaveric renal transplantation 19 years earlier. The patient was hypotensive on physical examination but without peripheral oedema, neck vein distention or hepatomegaly. It is noted that constrictive pericarditis (CP) are suggested by the presence of pericardial calcification in patients with symptoms and signs of heart failure.

Metabolic alkalosis is a rare occurence in hemodialysis population compared to metabolic acidosis unless some precipitating factors such as nasogastric suction, vomiting and alkali ingestion or infusion are present. When metabolic alkalosis develops, it may cause serious clinical consequences among them are sleep apnea, resistent hypertension, dysrhythmia and seizures. Here, we present a 54-year-old female hemodialysis patient who developed a severe metabolic alkalosis due to baking soda ingestion to relieve dyspepsia. She had sleep apnea, volume overload and uncontrolled hypertension due to metabolic alkalosis. Metabolic alkalosis was corrected and the patient's clinical condition was relieved with negative-bicarbonate hemodialysis [ABSTRACT FROM PUBLISHER]