Effect of cerebral microhemorrhages on neurocognitive functions in patients with end-stage renal disease.

BACKGROUND: Death is the most serious complication of intracerebral hemorrhage. Microbleeding can be a precursor of intracerebral hemorrhage. Susceptibility weighted imaging (SWI) should be included in imaging protocols for some specific groups such diabetic hemodialysis patients in terms of prediction of macrohemorrhages. PURPOSE: To investigate intracerebral microbleeding in hemodialysis patients and the correlation between microbleeding and neurocognitive impairment. MATERIAL AND METHODS: Forty-nine hemodialysis cases were involved in the study. Locations of microbleeding, correlation between microbleeding and hypertension, diabetes mellitus (DM), age, and duration of dialysis were analyzed. Standardized mini-mental test was performed. The tested cases were divided into two groups: intracerebral microbleeding (group 1, n = 26) and without intracerebral microbleeding (group 2, n = 17). RESULTS: Incidence of microbleeding and macrohemorrhage was noted as 59% and 14%, respectively, in all cases. All macrohemorrhagic cases also have microbleeding. In group 1, neurocognitive impairment was detected in 10 (38.4%) cases: six and four cases with moderate and mild impairment, respectively. In group 2, neurocognitive impairment was detected in 2 (11.7%) cases, both with mild impairment. A significant positive correlation was detected between microbleeding and neurocognitive impairment (P = 0.031). Although there was no correlation between attention disorder and microbleeding, a positive correlation was detected between close memory impairment and microbleeding (P = 0.027). A positive correlation was detected between DM and microbleeding (P = 0.027). CONCLUSION: In hemodialysis patients, microbleeding can be a cause of neurocognitive impairment which will be important for guide to treatment protocols. SWI should be included in the imaging protocol of diabetic hemodialysis patients with neurocognitive deterioration.

Effects of fasting during the month of Ramadan on renal function in patients with autosomal dominant polycystic kidney disease
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BACKGROUND: In this study, we aimed to examine the impact of fasting during the month of Ramadan on autosomal dominant polycystic kidney disease (-ADPKD) patients with normal to near-normal glomerular filtration rate (GFR). MATERIALS AND METHODS: This was a prospective observational study of patients with ADPKD, the majority of whom had normal or near-normal GFR. Patients were divided into two groups: the fasting group (FG) and the nonfasting group (NFG). Assessments in the NFG were performed 1 week before and 1 month after Ramadan, while FG patients were assessed on the last day of fasting in addition to the abovementioned visits. The following parameters were checked at each visit: blood pressure (BP), weight, sodium, potassium, blood urea nitrogen (BUN), creatinine, calcium, phosphorus, glucose, lipid profile, bicarbonate, urine density, 24-hour urine volume, 24-hour urine protein, GFR, neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1). Kidney function tests were carried out on the 7th day of fasting in the FG for the identification of early kidney damage. RESULTS: Of the overall group of 54 patients, 23 were in FG (19 female) and 31 were in NFG (18 female). There were no significant differences between the two groups in terms of age, gender, ADPKD duration, and presence of hypertension. The mean estimated glomerular filtration rate (eGFR) values of FG and NFG were 86.4 ± 18.5 and 66.1 ± 36.5 mL/min/1.73m2, respectively. During the follow-up period, no significant changes occurred in BP, weight, creatinine, 24-hour urine volume, NGAL, KIM-1, or GFR in either group (p > 0.05), while 24-hour urinary protein was significantly decreased in FG (p < 0.001). CONCLUSION: A fasting duration of ~ 17 hours a day did not affect renal function negatively in patients with early-stage chronic kidney disease due to ADPKD. Also, no significant changes occurred in acute renal failure markers.
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Endocan and albuminuria in type 2 diabetes mellitus.

BACKGROUND: Endocan is a newly identified proteoglycan released from endothelium, stimulating angiogenesis and when increased, indicates endothelial activation (inflammation). Our aim was to examine the association between serum endocan levels and urine albumin-creatinine ratio (UACR). METHOD: One hundred and thirty-seven patients with type 2 diabetes mellitus and normal serum creatinine who had no co-morbidities other than hypertension, diabetic nephropathy, retinopathy, or neuropathy were divided into normoalbuminuria (G1), microalbuminuria (G2), and macroalbuminuria (G3) groups and compared cross-sectionally regarding serum endocan levels. RESULT: There were 55, 47, and 35 patients in G1, G2, and G3, respectively. The groups were comparable in terms of gender, age, duration of diabetes, diabetic neuropathy/retinopathy, fasting glucose, HbA1c, serum creatinine level, and eGFR. Patients in G3 had significantly higher blood pressure but lower serum albumin and endocan levels. UACR showed a negative bivariate correlation with serum endocan levels (r = -.282, p = .001). There was bivariate positive correlation between endocan and systolic blood pressure (r=.185, p = .030). In linear regression analysis, UACR was negatively correlated with endocan while positively correlated with systolic blood pressure, duration of diabetes, and platelet distribution width. CONCLUSION: Patients with macroalbuminuria had lower endocan levels, and increasing UACR was associated with decreasing serum endocan levels. Despite the occurrence of angiogenesis and glomerular hypertrophy in the early phase of diabetic nephropathy, ensuing significant renal injury over time may reduce the expression of endocan. Serum endocan levels may represent a novel marker for nephropathy progression.

GAS6 intron 8 c.834 + 7G > A gene polymorphism in diabetic nephropathy.

UNLABELLED: BACKGROUND - AIM: In animal experiments, growth arrest-specific 6 (Gas6) protein plays a key role in the development of mesangial cell and glomerular hypertrophy in the early phase of diabetic nephropathy, and diabetic nephropathy is prevented by warfarin-induced inhibition of GAS6 protein. It was shown that GAS6 intron 8 c.834 + 7G > A polymorphism is protective against type 2 diabetes mellitus, and AA genotype is associated with higher blood levels of GAS6 protein. Our aim is to investigate whether this polymorphism is a risk factor for diabetic nephropathy in type 2 diabetes mellitus. METHOD: Eighty-seven patients with diabetic nephropathy were compared with 66 non-diabetic controls in terms of GAS6 intron 8 c.834 + 7G > A polymorphism. Patients with history of stroke, ischemic heart disease were excluded. Each patient was examined by the ophthalmologist to determine diabetic retinopathy. RESULTS: Frequency of GG, GA and AA genotypes are similar in diabetic nephropathy and control groups according to GAS6 intron 8 c.834 + 7G > A polymorphism (p = .837). Rate of diabetic retinopathy was 54.02%. In the subgroup analysis, GA genotype was significantly more frequent than GG genotype in patients with diabetic retinopathy when compared to without diabetic retinopathy (p = .010). CONCLUSION: In our study, GAS6 intron 8 c.834 + 7G > A polymorphism was not associated with diabetic nephropathy in type 2 diabetes mellitus. However, heterozygous state of this polymorphism may be a risk factor for diabetic retinopathy in patients with diabetic nephropathy.

The course of hypercalciuria and related markers of bone metabolism parameters associated with corticosteroid treatment.

BACKGROUND AND OBJECTIVE: Prolonged corticosteroid (CS) use induces osteoporosis; the pathogenesis of this condition is multifactorial and includes CS-induced hypercalciuria. We investigated the course of hypercalciuria and related markers of bone metabolism parameters during and after the CS treatment. MATERIALS AND METHODS: We recruited 42 patients who were taking at least 10 mg/day of methylprednisolone or an equivalent dose of CSs for at least 30 days. The 24-h urinary calcium and sodium, a spot urinary calcium/creatinine ratio, and urinary deoxypyridinoline were measured prior to the treatment, at day 7, at days 30-60, and after the cessation of the treatment. Additionally, the serum levels of phosphorus, calcium, alkaline phosphatase (ALP), albumin, creatinine, osteocalcin, and parathyroid hormone (PTH) were analyzed. RESULTS: The 24-h urinary calcium excretion was significantly increased at day 7 (182.2 ± 158.6 mg/day; p < 0.001) and at days 30-60 (196.9 ± 167.8 mg/day; p < 0.001) compared with baseline (98.7 ± 88.1 mg/day) and returned to basal level after the cessation of the CSs (118.9 ± 90.2 mg/day; p = 0.725). The urinary deoxypyridinoline level was significantly higher at days 30-60 compared with basal level. The serum osteocalcin level was decreased at days 30-60 when compared with day 7. No significant changes were detected in the PTH, phosphorus, creatinine, and ALP levels. CONCLUSIONS: CS treatment induces hypercalciuria just after starting the treatment until the end of it. CS-induced hypercalciuria promptly improved after cessation of the treatment. By days 30-60, the excretion of urinary deoxypyridinoline was accompanied by hypercalciuria. The serum osteocalcin level was decreased at days 30-60 when compared with day 7.

Fenofibrate-induced rhabdomyolysis in a patient with stage 4 chronic renal failure due to diabetes mellitus.

Rhabdomyolysis is defined as a pathological condition of skeletal muscle cell damage leading to the release of toxic intracellular components into the circulation. Several factors may lead to rhabdomyolysis. Fenofibrate is a fibric acid derivative agent that is used in the treatment of hyperlipidaemia. Although several case reports of rhabdomyolysis have been reported due to the combination of statin and fenofibrate, fenofibrate alone rarely causes rhabdomyolysis. When administering fenofibrate in chronic renal failure, dose should be adjusted. Here, we report a case with fenofibrate-induced rhabdomyolysis in a patient with chronic renal failure.

Relationship between visfatin and some clinical and biochemical parametres in peritoneal dialysis patients.

OBJECTIVE: To characterise the relationship between visfatin levels and various clinical and biochemical parameters in peritoneal dialysis patients. METHODS: The case-control study was conducted at the Medical Faculty Hospital, Yuzuncu Yil University, Van, Turkey, between May 2007 and December 2008, and involving 41 patients on peritoneal dialysis, 20 haemodialysis patients and 20 healthy controls. Fasting visfatin level was measured with enzyme-linked immunosorpent assay (ELISA) method, and patients on peritoneal dialysis were separated into two groups according to the visfatin levels - high and low. The groups were compared in terms of some clinical (height, weight, body mass index, waist circumference, hip circumference, waist/hip ratio, heart rate, systolic and diastolic blood pressure and the kt/V and CrCI (creatanine clearance) parameters which are indicative of the dialysis adequacy) and biochemical parameters (glucose, triglycerides, cholesterol, low density lipoprotein, high density lipoprotein, aspartate aminotransferase, alanine transminase, blood urea nitrogen, creatinine, total protein, albumin, globulin, sodium, potassium, magnesium, calcium, phosphorus, ferritin, venous blood gas, parathyroid hormone and insulin). SPSS 15 was used for statistcal analysis. RESULTS: No statistically significant difference in the visfatin levels was found between the patients and controls (7.71 +/- 4.04, 7.36 +/- 3.71, 7.70 +/- 1.61, respectively, p = 0.63). The triglyceride level of the high-visfatin group was significantly higher than that of the low-visfatin group (243.8 +/- 133.2, 150.8 +/- 65.8, respectively, p<0.05). However, there was no correlation between visfatin and triglyceride levels. No difference in the other clinical and biochemical parametres was observed between the two groups of peritoneal dialysis patients. CONCLUSIONS: No significant difference in the serum visfatin levels of peritoneal dialysis patients compared to haemodialysis patients or healthy individuals was noticed. Further studies are needed to confirm the effect of visfatin on triglyceride levels, and, if confirmed, the mechanism of this relation.

The importance of oxidative stress in patients with chronic renal failure whose hypertension is treated with peritoneal dialysis.

Increased oxidative stress is a well-known phenomenon in dialysis patients. However, the contribution of hypertension to the oxidative stress in peritoneal dialysis patients has not yet been assessed. The present study aimed to investigate if hypertension had an additional effect on oxidative stress in peritoneal dialysis patients. A total of 50 patients treated with peritoneal dialysis were divided into two groups: The patients with mean of last three blood pressure results as 135/90 mmHg and above were considered hypertensive, the patients with lower blood pressure were considered normotensive. The control group included 25 healthy individuals. Serum malondialdehyde (MDA), advanced oxidation protein product (AOPP), myeloperoxidase (MPO), catalase (CAT) and glutathione peroxidase (GSH-Px) levels were measured in all groups. MDA level, an indicator of lipid peroxidation, was significantly higher in the hypertensive group compared to the control group, while the increase in the normotensive group was not significant. However, the difference between the hypertensive and normotensive groups was significant. The levels of AOPP, an indicator of protein oxidation level, and MPO, an indicator of neutrophil activation, were not different between the groups, while the activities of antioxidant CAT and GSH-Px decreased in both normotensive and hypertensive groups compared to the control group, and there was no significant difference between the patient groups. This study shows that both normotensive and hypertensive peritoneal dialysis patients have increased-oxidative stress and decreased antioxidant levels and hypertension might have an additional effect on oxidative stress by increasing MDA level in peritoneal dialysis patients.

Polyneuropathy due to cyclosporine A in patients with renal transplantation: a case report.

BACKGROUND: Calcineurin inhibitor cyclosporine A (CsA) is a potent immunosuppressive agent. The side effects of CsA include nephrotoxicity, hypertension, hypertrichosis, infection, hyperpotassemia, and, to a lower extent, neuropathy. OBJECTIVES: In this case report, we aimed to present a renal transplant patient with polyneuropathy (PNP) due to the use of CsA and with improvement when switched to rapamycin. METHODS: In electromyography, axonal sensory PNP was detected. CsA was stopped and rapamycin was begun. RESULTS: His complaints rapidly improved after using rapamycin. CONCLUSIONS: Patients using CsA should be closely monitored for peripheral neuropathy and in case of toxicity, alternative immunosuppressive agents should be considered.

Investigation of the relationship between serum levels of cotinine and the renal function in active and passive smokers.

OBJECTIVE: We have investigated the effects of active and passive smoking on renal functions in terms of glomerular filtration rate, microalbuminuria, and ß-2 microglobulin excretion. DESIGN AND METHOD: The volunteers included in this study were classified into three groups as active smokers (n = 24), passive smokers (n = 20), and controls (n = 20). Blood and urine samples were collected from all groups. Serum glucose, urea, creatinine, and cotinine levels in the collected blood samples were measured. Also, microalbumin, ß-2 microglobulin, and creatinine levels were measured in the collected urine samples. RESULTS: Serum cotinine levels were found to be higher in both passive and active smokers when compared with controls ( p < 0.01), whereas urinary microalbumin and creatinine levels were significantly higher in active smokers ( p < 0.01). The urinary microalbumin/creatinine ratio was significantly increased in both active and passive smokers compared with controls. CONCLUSION: The kidney and the glomerular functions may be affected even by passive smoking. In addition, increased microalbumin/creatinine ratio may be a sign of increased atherosclerosis risk in these persons.

Successful management of membranoproliferative glomerulonephritis type I in pregnancy.

PURPOSE: We report the successful management of a pregnancy with preexisting nephrotic syndrome due to biopsy-proven primary membranoproliferative glomerulonephritis type I. METHODS: A 21-year-old Turkish woman with membranoproliferative glomerulonephritis type I was followed up by the obstetrics and gynecology, and nephrology departments of a university hospital throughout her pregnancy starting from the 25th week of gestation. RESULTS: Due to progression of intrauterine growth retardation and fetal distress, a cesarean section was performed in the 33rd week of gestation. Although creatinine was unchanged, proteinuria increased with relatively stable albumin levels 3 months after delivery and her treatment was adjusted accordingly. CONCLUSIONS: If the mother is not suffering from hypertension or renal insufficiency, specific therapy for membranoproliferative glomerulonephritis type I during pregnancy provided by a nephrologist together with regular obstetric care may allow the patient to have a viable fetus, which might be growth retarded if proteinuria is increased.

Comparative effects of carvedilol and lercanidipine on ultrafiltration and solute transport in CAPD patients.

BACKGROUND: Peritonitis, the type of buffer used in the dialysate, continue ambulatory peritoneal dialysis (CAPD) of greater than two years duration, increased exposure to dialysate glucose, diabetes mellitus, and the use of beta blockers may contribute to impaired ultrafiltration. OBJECTIVES: The aim of the present study is to compare the effects of a calcium-channel blocker and a beta-blocker on the peritoneal transport and clearance. METHODS: We studied 48 patients with ESRD on chronic peritoneal dialysis, included 27 females and 19 males with mean age 42.6 +/- 16.4 years. Two patients were excluded from the study due to peritonitis. Patients were treated either with carvedilol or lercanidipine. In all patients; peritoneal equilibration test (PET), ultrafiltration (UF), Kt/V ratio, creatinine clearance (CrCl), systolic blood pressure, diastolic blood pressure, serum BUN, creatinine, glucose, sodium, potassium, albumin, cholesterol, and triglyceride values were obtained before and after 8 weeks from the start of the drug treatment. RESULTS: Lercanidipine and carvedilol showed a good antihypertensive effect in CAPD patients. Both drugs had a good tolerability profile and showed no effect on plasma lipids. There were no differences in terms of PET, ultrafiltration, Kt/V ratio, CrCl, systolic blood pressure, diastolic blood pressure, serum BUN, creatinine, glucose, sodium, and potassium values between both patient groups. After antihypertensive treatment, neither group showed a difference in the above-mentioned parameters (p > 0.05) except potassium, which was significantly higher in the carvedilol group (p < 0.05). CONCLUSIONS: In CAPD patients. short-term usage of carvedilol has no effect on ultrafiltration and solute transport like lercanidipine. Both drugs showed a good antihypertensive effect.

Trace element status of chronic renal patients undergoing hemodialysis.

The purpose of this study was to examine the status of trace elements (Cu, Zn, and Fe) and minerals (Mg, K, Na, and Cl) and the level of biochemical parameters (urea, creatinine, total protein, albumin, and glucose) in hemodialysis (HD) patients. This study included 30 HD patients (25 men and 5 women) aged 52.12 +/- 3.13 years and 30 healthy subjects (23 men and 7 women) aged 51.64 +/- 2.22 years. This study investigated the status of trace elements and minerals in HD patients. It was found that the total HD patients (before and after dialysis) had statistically lower Zn and albumin in the after-dialysis group K and Cl levels and higher Mg, creatinine, and urea in the before-dialysis group K and in the after-dialysis group glucose levels than those of the controls. It was determined that the results might be helpful in monitoring patients with renal failure in terms of insufficiency or excess of trace elements and minerals. There was positive correlation for Mg-K (r = 0.64; p = 0.001), creatinine-urea (r = 0.59; p = 0.001), K-urea (r = 0.56; p = 0.001), K-creatinine (r = 0.52; p = 0.003), Mg-creatinine (r = 0.47; p = 0.008), Zn-albumin (r = 0.40; p = 0.028), and Zn-creatinine (r = 0.40; p = 0.031) in the before-dialysis session. There was also positive correlation for creatinine-urea (r = 0.56; p = 0.001), K-urea (r = 0.39; p = 0.035), and Mg-creatinine (r = 0.38; p = 0.041) in the after-analysis session. As a result of the analysis of regression between serum levels of albumin and zinc in total HD patients, the use of the level of albumin might be a suitable choice in determining zinc deficiency resulting from the decrease in the level of zinc in parallel to that of albumin. The results also suggest that the relationship between creatinine and K, Mg, and Zn could be ascribed to the loss of renal function.

Effect of depot oral cholecalciferol treatment on secondary hyperparathyroidism in stage 3 and stage 4 chronic kidney diseases patients.

By the time patients require dialysis replacement therapy, nearly all chronic kidney diseases (CKD) patients are affected with uremic bone diseases. High-turnover osteodystrophy can be prevented; patients with CKD should be monitored for imbalances in calcidiol (25 OH vitamin D), calcium, and phosphate homeostasis. We aimed to determine the effect of a monthly oral 300,000 IU vitamin D(3) (cholecalciferol) supplementation on the uremic bone diseases (UBD) markers such as iPTH and alkaline phosphatase in CKD patients. Among a total of 70 patients under treatment in the nephrology unit, 40 predialysis CKD patients (mean age of 49 +/- 14, male/female 20/20) were included the study. The patients were randomly divided into two groups. Treatment group included 20 patients (mean age of 51 +/- 14, male/female 9/11), and the control group comprised 20 patients (mean age of 47 +/- 14, male/female 9/11). Treatment group patients were given a single dose of Devit3 ampoule (300,000 U cholecalciferol) per month orally way. Patients in the control group did not take any vitamin D for a month. The level of calcidiol was lower than normal range in two groups. After a month, treatment group patient's calcidiol increased statistically significant (6.8 +/- 3.5 to 17.8 +/- 21.4 ng/mL, p < 0.001). After a month, iPTH level decreased in the treatment group statistically significantly (368 +/- 274 to 279 +/- 179 pg/ml, p < 0.001). At the 30(th) day of the treatment, in 9/20 of the treatment group patients (45%), the iPTH value decreased at least 30% (p < 0.001). We suggest that oral depot cholecalciferol treatment causes a statistically significant decrease of serum iPTH level but does not cause a statistically significant change in Ca, P, ratio of Ca x P, or urinary calcium creatinine rate in UBD predialysis CKD. This treatment can be used safely for the predialysis CKD patients, along with the cautious control of serum calcium and phosphor.

Diurnal rhythm of urinary calcium excretion in adults.

Twenty-four-hour urinary calcium excretion is normally the equivalent of daily calcium intake, and varies between 200-300 mg/dL with a calcium/creatinine ratio of 0.07-0.15. In this study, we aimed to investigate the diurnal rhythm of calcium excretion in healthy individual. Forty subjects (30 male, 10 female) were involved into the study. The spot urine samples were taken at 08:00, 14:00, and 22:00 together with a 24-hour collection. Mean spot urinary calcium levels at 08:00, 14:00, and 22:00 were 12.39 +/- 8.19, 12.97 +/- 8.37, and 16.95 +/- 10.39 mg/dL, with calcium/creatinine ratios of 0.104 +/- 5.261, 0.119 +/- 7.85, and 0.133 +/- 8.17, respectively. Twenty-four-hour urinary calcium excretion was 12.74 +/- 7.31 mg/dL with a calcium/creatinine ratio of 0.111 +/- 5.41. The values at 08:00, 14:00, and of 24-hour collection were statistically similar (p > 0.05), but the nighttime values were significantly elevated (p < 0.05). In conclusion, calcium excretion is increased at night, and urinary calcium measurements should be interpreted accordingly.

Protective effect of dexpanthenol against nephrotoxic effect of amikacin: An experimental study.

BACKGROUND: Amikacin has the largest spectrum among aminoglycosides, its nephrotoxic effect limits its utilization. Our purpose in this study is to review the protective effect of dexpanthenol against the nephrotoxic effect of amikacin, accompanied with histopathological and biochemical parameters. METHODS: 32 rats were randomly separated into four groups with eight in each (amikacin (1.2mg/kg/day), amikacin (1.2mg/kg/day)+dexpanthenol (500mg/kg/day), dexpanthenol (500mg/kg/day) and control). In order to assess the oxidative balance and renal damage between groups, biochemical parameters (total antioxidant capacity (TAS), total oxidant stress (TOS), catalase (CAT), paraoxonase (PON), arylesterase (ARES), urea, and creatinin) were studied from the blood samples. At the end of the 14th day, renal tissues were reviewed blindly by a pathologist. RESULTS: TOS and oxidative stress index (OSI) values were significantly lower in the group which was administered with dexpanthenol+amikacin compared to the group which only received amikacin (respectively, p=0.001, p=0.002). Antioxidant biochemical parameters (TAS, CAT, PON, and ARES) were significantly higher in the group which was administered with dexpanthenol+amikacin compared to the group administered only with amikacin (respectively, p=0.007, p=0.001, p=0.003, p=0.003). Urea and creatitin values were found to be significantly lower in the group which was administered with dexpanthenol+amikacin compared to the group administered only with amikacin (respectively, p=0.002, p=0.001). Histopathologic changes such as glomerular and tubular epithelium changes and interstitial edema were clearly observed in the group administered only with amikacin, such findings were insignificant in the group administered with dexpanthenol+amikacin. CONCLUSION: It was revealed with biochemical and histopathologic data that nephrotoxic effects created by amikacin administration can be limited with dexpanthenol by using them together, and further advanced clinical studies are required.

Effect of cyproheptadine on serum leptin levels.

Leptin is a 167 amino acid protein encoded by the obesity gene that is synthesized in adipose tissue and interacts with receptors in the hypothalamus linked to the regulation of appetite and metabolism. It is known to suppress appetite and increase energy expenditure. Cyproheptadine is a piperidine antihistamine that increases appetite through its antiserotonergic effect on 5-HT2 receptors in the brain. Although both leptin and cyproheptadine are effective in controlling appetite, their interaction has not been addressed in clinical studies. This study evaluated serum leptin concentrations in patients who received cyproheptadine to treat a variety of disorders. Sixteen patients aged 7 to 71 years (mean, 26.25 years) were given cyproheptadine 2 to 6 mg/day for a minimum of 7 days. Body weight was measured and blood samples were obtained at baseline and after 1 week of treatment. Serum leptin levels were determined by leptin radioimmunoassay. The mean body weight at baseline (52.59 kg) did not differ significantly from that at 1 week after treatment (52.84 kg; P > .05), but the mean leptin level after 1 week of treatment with cyproheptadine (3.14 ng/mL) was 14.2% higher than that at baseline (2.75 ng/mL; P < .05). This increase may suggest that both leptin and cyproheptadine may affect appetite via similar receptors and that cyproheptadine does not impair leptin activity through these receptors. Further study will be necessary to clarify this relationship.

Nonketotic hyperosmolar coma in a patient with type 1 diabetes-related diabetic nephropathy: case report.

Nonketotic hyperosmolar coma (NHC) is characterized by severe hyperglycemia; absence of, or only slight ketosis; nonketotic acidosis; severe dehydration; depressed sensorium or frank coma; and various neurologic signs. This condition is uncommon in type 1 diabetes. Because of little or no osmotic diuresis in patients with diabetic nephropathy, increases in plasma osmolality and therefore the likelihood of neurologic symptoms are limited. A 20-year-old male patient with type 1 diabetes with chronic kidney disease on conservative treatment (glomerular filtration rate [GFR], 18 mL/dk) presented with acute nonketotic hyperosmolar syndrome. The patient was admitted presenting with thirst, fatigue, and drowsiness. Blood biochemistry levels were urea 87 mg/dL, creatinine 5.09 mg/dL, glucose 830 mg/dL, glycosylated hemoglobin (HbA1c) 8%, C peptide <0.3 ng/mL, sodium 131 mmol/L, chloride 93 mmol/L, potassium 5.2 mmol/L, and calculated serum osmolality 385 mOsm/kg. The presumptive diagnosis on admission was nonketotic hyperosmolar syndrome precipitated by urinary infection. This is the first case report of hyperosmolar coma in a patient with type 1 diabetes with chronic kidney disease.

Incidence of renal insufficiency in cancer patients.

The frequency of chronic renal insufficiency among cancer patients is unclear. The aim of this study was to determine the frequency of impaired renal function within a population of cancer patients. One thousand two hundred seventeen patients (563 women, 654 men) with cancer underwent serum creatinine concentration and glomerular filtration rate (GFR) evaluations. The Cockcroft-Gault formula was used to estimate the GFR from the creatinine clearance (Cl(cr)). Renal insufficiency was defined as a GFR 1.2 mg/dL). According to the Cockcroft-Gault formula evaluations, however, 330 (27.1%) of the patients had an estimated GFR <90 mL/min. Among these, the Clcr was between 60 and 89 mL/min in 241 patients (19.8%); 30 and 59 mL/min in 75 patients (6.2%); and 15 and 29 mL/min in 7 patients (0.6%); 7 patients (6%) had a Cl(cr) <15 mL/min. As a result, 21.2% of patients demonstrating a normal serum creatinine level had abnormal renal function. Renal function should be evaluated in all cancer patients, regardless of their serum creatinine level, before any drug regimen is administered. The Cockcroft-Gault formula appears to be more accurate than serum creatinine concentration for diagnosing renal insufficiency in patients with cancer, but more prospective studies in this population will be necessary to confirm this finding.

Fatal lactic acidosis due to leukemic transformation in a patient with non-Hodgkin's lymphoma: case report.

Lactic acidosis (LA) associated with hematologic malignancies is uncommon, life-threatening, and generally occurs in adults. Its pathogenesis is poorly understood. This is a case report of LA due to leukemic transformation that occurred in a patient with non-Hodgkin's lymphoma (NHL). A 24-year-old man with NHL was admitted to the hospital with dyspnea. Venous blood gas analysis revealed metabolic acidosis (pH 7.05; HCO3 6 mEq/L; BE 22 mmol/L; anion gap 28 mEq/L); the patient had an elevated plasma lactate concentration (12 mmol/L) and low glucose concentration (38 mg/dL). There was no reason other than leukemia-such as infection, circulatory failure, or drug use-for the development of severe LA. This case report shows that in patients with NHL, leukemic transformation may give rise to LA.