Mevlut Ceri

Acute Kidney Injury due to Rhabdomyolysis in H1N1 Influenza Infection

Acute kidney injury (AKI) is rarely reported in the clinical course of H1N1 infection and this condition is strongly related with increasing of mortality risk. However, there are no sufficient data about the development of AKI due to H1N1 infections. The recent reports were documented for elevation of creatinine phosphokinase levels in the course of influenza infection, but rhabdomyolysis was rarely reported. Herein, we present a 28-year-old female patient and a 19-year-old male patient with AKI in the course of H1N1 influenza infection due to rhabdomyolysis.

Comment on: low-dose quetiapine-induced severe rhabdomyolysis.

There are only few severe rhabdomyolysis reports following quetiapine overdose and therapeutic dosage.1–4 Here, we report a case of developing rhabdomyolysis after 6 months of quetiapine therapy. To our knowledge, this is the first case to describe rhabdomyolysis in a quetiapine-treated patient with chronic kidney disease taking therapeutic dosage. A 54-year-old man was admitted to the hospital with nausea, vomiting, myalgias, weakness of both hands and lower limb that caused a reduction in everyday activity for 10 days. He had a known medical history of chronic renal disease, coronary artery disease, hypertension, cerebrovascular disease, anxiety, and bipolar depression. He was treated with 20 mg/day of escitalopram supplementary to quetiapine 25 mg/day because of anxiety and bipolar depression 6 months ago. Moreover, medications included metoprolol 50 mg/day, olmesartan 10 mg/day, and acetylsalicylic acid 100 mg/ day. Both his physical examination and ECG (QTc interval) were normal. The patient’s laboratory findings were as follows: blood urea nitrogen 19.6 mmol/L, creatinine 264 μmol/L, creatinine phosphokinase (CPK) 3865 U/L (normal 0–170), aspartate aminotransferase (AST) 162 U/L, alanine aminotransferase (ALT) 75 U/L, and myoglobin 3157 ng/mL (normal 0–38.5); other laboratory values were within normal ranges. Urine dipstick chemical analysis suggested moderate blood presence but there were no erythrocytes identified by microscopic examination, suggesting myoglobulinuria. Serum quetiapine tests could not be performed because of technical difficulties. The patient was diagnosed with rhabdomyolysis based on his clinical presentation and laboratory values. After exception of other causes of rhabdomyolysis, quetiapine was discontinued. He was given extensive hydration including intravenous normal saline with bicarbonate. On the fourth admission day, CPK, AST, and ALT levels had dropped to 1272, 128, 68 U/L, respectively. Serum myoglobin was decreased to 566 ng/mL and serum creatinine decreased to 202 μmol/L. CPK, AST, ALT, and myoglobin were returned to normal levels after ten days. Our patient, who had no evidence of seizure or hints for intoxication, had depressive episodes for years and took escitalopram before. CPK level rapidly turned normal after quetiapine discontinued. Therefore, this patient was considered as rhabdomyolysis due to quetiapine treatment. The new generation antipsychotics (NGAs) are frequently prescribed as first-line drugs in the treatment of psychotic and mood disorders. CPK elevation has been observed during treatment with NGAs such as clozapine, loxapine, or olanzapine.5 However, only few cases about rhabdomyolysis associated with quetiapine have been reported so far.1–4 We described the first case of quetiapine-induced rhabdomyolysis in a patient with chronic renal disease. Quetiapine is primarily metabolized by sulfoxidation and oxidation with the cytochrome P450 (CYP) 3A4 isoenzyme and the 7-hydroxylated and the N-dealkylated metabolites are pharmacologically active.6 Escitalopram is metabolized by the CYP isoenzymes CYP2C19, CYP2D6, and CYP3A4. The combination of quetiapine with escitalopram may inhibit the elimination of quetiapine and consequently may increase drug level. One possible pathophysiological hypothesis explains CPK elevation during antipsychotic treatment as the result of a dysregulated sympathetic nervous system. According to this hypothesis, the inhibition of the sympathetic nervous system by dopaminergic neurons is suppressed by antipsychotic agents, and overdoses of catecholamines have been shown to lead to muscle cell necrosis.3 Moreover, our patient might have had a tendency to rhabdomyolysis because of having chronic kidney disease. In conclusion, NGAs are replacing traditional antipsychotics and are widely prescribed by clinicians. If there is a patient complaining about muscle pain during therapy with quetiapine, rhabdomyolysis should be suspected. In this situation, we suggest to have monitored closely muscle enzymes and renal functions, especially in patients with chronic kidney disease, while discontinuing quetiapine.

Behcet's disease and IgA nephropathy.

Although Behçet’s disease (BD) is a kind of systemic disease, renal involvement is rare, especially IgA nephropathy (IgAN). Renal manifestations in BD range from mild urinary abnormalities to glomerulonephritis with persistent renal failure, which includes minimal change disease, proliferative glomerulonephritis, rapidly crescentic glomerulonephritis, renal amyloidosis and IgA nephropathy. Amyloidosis seems to be the most common type of renal lesion in BD, and several cases of nephrotic syndrome secondary to amyloidosis have been documented. Co-occurrence of BD and IgA nephropathy has only been reported in only few cases. We describe two patients with the rare association of BD and IgAN. We suggested that it is important to periodically perform renal function assessment in patients with BD, through urinalysis and measurement of serum creatinine for detecting any abnormality and providing an early adequate treatment.

Is colchicine therapy effective in all patients with secondary amyloidosis

Abstract Objective: Although colchicine is effective on prevention and regression of amyloidosis in many cases, rate of unresponsiveness to colchicine therapy is not too low. However, there is no sufficient data about which factors effect to response of colchicine therapy on regression of amyloidosis. Materials and methods: 24 patients with renal amyloidosis were enrolled into the study. The patients were divided in two groups according to urinary protein excretions: non-nephrotic stage (14/24) and nephrotic stage (10/24). The patients were also categorized according to the etiology of amyloidosis; familial Mediterranean fever (FMF)-associated amyloidosis (15/24) versus rheumatoid disorders (RD)-associated amyloidosis (9/24). The changes of amount of proteinuria and estimated glomerular filtration rates were investigated after colchicine treatment started in these groups. Results: The mean follow-up period was 27.7 ± 19.2 months. After initiating colchicine therapy, the degree of proteinuria was decreased higher than 50% in 11/14 (78%) of non-nephrotic patients and elevated only in three (22%) patients. In nephrotic group, proteinuria was increased in 5/10 (50%) of patients. Glomerular filtration rates were stable in nephrotic and non-nephrotic groups. Presenting with nephrotic syndrome was higher in RD-associated amyloidosis (RD_A) group (5/9) than FMF-associated amyloidosis (FMF_A) group (5/15) without statistical significance (p > 0.05). After colchicine treatment, proteinuria was decreased in 12/15 patients in FMF_A group, however, the significant decreasing of proteinuria was not observed in RD_A group (p = 0.05 vs. p > 0.05). Conclusion: Colchicine therapy was found more effective in low proteinuric stage of amyloidosis. The beneficial effect of colchicine therapy was not observed in patients with RD- associated amyloidosis.

Effects of renin-angiotensin-aldosterone system blockade on chlorhexidine gluconate-induced sclerosing encapsulated peritonitis in rats.

Sclerosing encapsulated peritonitis (SEP) is a rare complication of long term peritoneal dialysis. Renin‐angiotensin‐aldosterone system (RAAS) may play a role in the development of peritoneal fibrosis in CAPD patients. We aimed to evaluate the effect of aliskiren, valsartan, and aliskiren + valsartan therapy on SEP. The study included 30 Wistar albino rats which were divided into five groups: I (Control) SF solution i.p.; II (CG group) chlorhexidine gluconate i.p.; III aliskiren oral plus CG i.p.; IV valsartan oral plus CG i.p.; and V aliskiren oral, valsartan oral and CG i.p. On the twenty‐first day, all of the rats were sacrificed. All of the groups were analyzed in terms of peritoneal thickness, degree of inflammation, vasculopathy, neovascularization and fibrosis. Also, the parietal peritoneal tissue samples were evaluated for matrix metalloproteinase 2 (MMP‐2) using the ELISA method. Peritoneal thickness and fibrosis scores were lower in the valsartan group compared to the CG group (P < 0.05). Peritoneal fibrosis scores were lower in the aliskiren group compared to CG group (P < 0.05) but no difference was observed between the peritoneal thickness scores of the two groups (P > 0.05). Tissue MMP‐2 levels were significantly higher in the CG group compared other groups (P < 0.05). There were no statistically significant differences between the aliskiren, valsartan and aliskiren + valsartan groups according to the tissue MMP‐2 levels. Due to the antifibrotic properties of valsartan, it is thought to be a possible choice to prevent SEP development. We found no positive impact of aliskiren or aliskiren + valsartan combination compared to valsartan alone.

An unusual cause of focal segmental glomerulosclerosis: psoriasis vulgaris

Psoriasis, being limited to the skin, is generally a chronic inflammatory disorder. Several glomerular diseases have been distinguished due to renal histological findings of psoriatic patients to date. The underlying pathogenetic mechanisms of these associations remain unclear because of the limited number of cases. We report a second case of focal segmental glomerulosclerosis in a psoriatic patient.

An unusual effect of colchicine treatment in familial Mediterranean fever-associated glomerulonephritis.

Kidney involvement is usually depend on amyloidosis in Familial mediterranean fever (FMF) and in most cases with glomerulonephritis has been reported [1]. Here, we report remission of proteinuria, which is observed with only regular colchicine treatment, is a case of IgA nephropathy in the course of FMF. A 27-year-old woman was admitted to our hospital because of proteinuria in urinary analysis. She has not regularly taken colchicine treatment who had been diagnosed FMF 15 years ago. The patient’s physical examination findings were normal. The patient’s laboratory findings were 5 erythrocytes identified by microscopic examination and proteinuria (619 mg/day), but others were normal. Percutaneous kidney biopsy was performed due to persistent proteinuria. The diagnosis of IgA nephropathy was made based on light and immunofluorescence microscopic assessment. Staining for amyloidosis was negative. After M694 V/M694 V homozygous mutation was confirming the diagnosis of FMF, regular colchicine treatment was begun (0.5 mg, t.i.d). Because of resolving proteinuria under colchicine treatment alone, immunosuppressive and ACEI/ARB therapies were not used. After taking regular treatment, the patient had no fever and abdominal pain attacks. In the following year, the patient’s creatinine 0.7 mg/dl, creatinine clearance 108 ml/min/ 1.73 m, and urinalysis were completely normal. FMF is an autosomal-recessive genetic disease affecting mainly Turks, non-Ashkenazi Jews, Armenians, and Arabs. It is characterized by recurrent attacks of fever and painful episodes of sterile poliserositis and less frequently erysipelas-like rash. MEFV, the gene responsible for the disease, is localized on the short arm of chromosome 16 and encodes a 781-amino acid protein known as pyrin or marenostrin that is expressed in matur neutrophils plays an essential role in the pressure of inflammation. Adversely, mutated pyrin associates with uncontrolled inflammation through interleukin-1b and NF-jB activation, resulting in up-regulation of inflammatory cytokines pathways [2]. Colchicine is effective in preventing the trigger of FMF attacks and to hinder subclinical inflammation preventing the deposition of amyloid fibrils. It binds to b-tubulin hindering its polarization with consequent defective intracellular transfer and mitosis, inhibition of neutrophil chemotaxis, and reduced expression of adhesion molecules [3]. In addition, it has antioxidant and antifibrotic properties, all of them might have contributed to the remission of proteinuria. In the literature up to now, many times glomerulonephritis associated with FMF has been reported, but there is less resolving proteinuria with colchicine therapy. Cagdas et al. reported was remission of a patient with mesengial proliferative glomerulonephritis occurred after 3 years who took regular treatment [4]. Gok et al. and Koukoui et al. have been reported the remission of FMF-related IgA nephropathy while taking colchicine therapy [5, 6]. Similarly, remission of our patient with IgA nephropathy and FMF was successful after taking 1-year colchicine therapy. In conclusion, several kinds of glomerular diseases can be seen in FMF, and FMF-associated glomerulonephritis M. Ceri (&) S. Unverdi R. Yılmaz M. Duranay Department of Nephrology, Ankara Education and Research Hospital, Cebeci, Ankara, Turkey e-mail: tscer@yahoo.com

Renal injury due to hepatic hydatid disease

BACKGROUND Many studies on renal hydatid disease have been reported in the literature, and the disease process appears to be well defined. However, renal injury without direct renal invasion remains poorly understood. The present study aims to define the frequency and the property of the renal involvement in hydatid disease. METHODS Eighty patients older than 18 years and diagnosed with liver echinococcosis were included in the study. The echinococcosis was diagnosed by the haemagglutination test and abdominal ultrasonography. Twenty-four-hour protein excretion was measured for patients who had elevated serum creatinine levels or whose urinalyses were positive for haematuria or proteinuria. Subsequently, renal biopsy was performed, and the specimens were examined by light microscopy and immunofluorescence staining. RESULTS Haematuria was detected in 11 patients (13.75%), and proteinuria was detected in nine patients (11.25%). Percutaneous renal biopsy was applied to nine patients who gave signed consents to undergo the test. We detected four immunoglobulin A nephritis (together with tubulointerstitial nephritis in one patient), one membranoproliferative glomerulonephritis, one immunoglobulin M nephritis together with mesangiocapillary glomerulonephritis, one membranous glomerulonephritis, one amyloidosis and one tubulointerstitial nephritis. Renal hydatid cyst was detected only in four patients (5%). CONCLUSIONS Hydatid disease, which affects the kidney, is not rare, and we suggest that urinalysis and, if indicated, renal biopsy should be performed for hepatic hydatid disease diagnosis.

Massive intracerebral hemorrhage associated with Wegener granulomatosis

Wegener granulomatosis (WG) is a necrotizing granulomatous vasculitis that predominantly affects airways and kidneys. But central nervous system involvement (7–11%) is an uncommon. Massive ICH may occur in the course of WG, and this serious condition is related with high risk of mortality. Therefore, the new treatment strategies may be considered in addition to classical practices in serious organ involvement and recurrent attack. Here, we present an adult patient with WG whose disease was complicated by a massive intracerebral hemorrhage (ICH), which subsequently led to death.

Focal segmental glomerulosclerosis in association with Gitelman syndrome

Gitelman syndrome (GS) is an autosomal recessive disorder characterized by hypokalemia, metabolic alkalosis, hypomagnesemia and hypocalciuria. Glomerulonephritis associated with GS is rarely documented in the literature. We present an adult patient with GS whose renal biopsy revealed focal segmental glomerulosclerosis.