Dean A. Kujubu

Prevalence of nondiabetic renal disease in diabetic patients.

Background: Diabetic nephropathy is the leading cause of end-stage renal disease in the USA, yet most patients with type 2 diabetes mellitus are not formally evaluated with a renal biopsy. Our aim was to evaluate the prevalence of nondiabetic renal disease (NDRD) in patients with type 2 diabetes mellitus to determine common clinical indicators suggestive of NDRD. Methods: A retrospective analysis was performed on biopsy reports of patients who had undergone native renal biopsy between January 1, 1995, and December 31, 2005. Results: After exclusion of 57 patients, 233 patients with DM2 were included in our analysis. Mean age at the time of biopsy was 58.1 ± 13.7 years, and 53.0% of the study population were male. There were 124 cases (53.2%) with a pathologic diagnosis of NDRD, 64 (27.5%) with pure diabetic glomerulosclerosis (DGS) and 45 (19.3%) with concurrent NDRD and DGS (CD). Patients with NDRD tended to be younger than those with DGS and had significantly less associated diabetic retinopathy. Focal segmental glomerulosclerosis was the most common lesion found in patients with NDRD and accounted for 21.0% of all NDRD, followed by minimal-change disease (15.3%). IgA nephropathy (15.6%) and membranous glomerulonephritis (13.3%) were the most prevalent lesions found in patients with CD. Conclusions: The high prevalence of NDRD found in our population underscores the need for clinicians to consider renal biopsy in diabetic patients with an atypical clinical course, since additional disease-specific therapies may be helpful for this subset of the population.

Sleep Apnea in Early and Advanced Chronic Kidney Disease* Kaiser Permanente Southern California Cohort

BACKGROUND Sleep apnea (SA) has been reported to be highly prevalent in the dialysis population. The reported rates of SA in dialysis are severalfold greater than the 2 to 4% estimated in the general population. This study sought to determine whether an association exists between SA and early stages of chronic kidney disease (CKD) where SA may represent an important comorbidity and potential risk factor in kidney disease. METHODS Cross-sectional study of adults from an integrated health plan with documented serum creatinine levels in the period January 1, 2002, through December 31, 2004. SA diagnosis determined by International Classification of Diseases, ninth revision, coding for SA and Current Procedural Terminology coding for positive airway pressure devices. Kidney function was determined by the estimated glomerular filtration rate (eGFR). Logistic was regression used to estimate the relative risk for SA. RESULTS The overall prevalence of SA was 2.5% in the study population that included subjects with normal renal function and those with CKD. The odds ratios (ORs) for SA by eGFRs of 75 to 89, 60 to 74, 45 to 59, 30 to 44, and 15 to 29 mL/min per 1.73 m(2), respectively, compared to normal kidney function, after adjustment for age, sex, and number of visits, were as follows: 1.22 (95% confidence interval [CI], 1.18 to 1.25); 1.32 (95% CI, 1.27 to 1.37); 1.42 (95% CI, 1.35 to 1.50); 1.37 (95% CI, 1.25 to 1.50); and 1.32 (95% CI, 1.13 to 1.55). The increased ORs for eGFRs > 45 mL/min per 1.73 m(2) were sustained even after controlling for diabetes, heart failure, and hypertension. CONCLUSION This study demonstrated an increased risk of SA in patients with early CKD. Further evidence of a causal relationship should be sought in the hope that the detection and management of SA may improve the course of CKD.

25-Hydroxyvitamin D Levels and Hypertension Rates

Vitamin D deficiency has been linked to cardiovascular disease and risk factors including hypertension. The authors sought to determine prevalence rates of hypertension in adults tested for 25‐hydroxyvitamin D categorized by their levels and evaluate odds ratios for hypertension at lower 25‐hydroxyvitamin D levels compared with optimal levels. A cross‐sectional study was conducted January 1, 2004, through December 31, 2006, of patients aged 18 years and older within a large ethnically diverse population. Diagnosis of hypertension was determined by International Statistical Classification of Diseases and Related Health Problems codes. Patients were categorized into quartiles according to 25‐hydroxyvitamin D levels: ideal (≥40 ng/mL), adequate (30–39 ng/mL), deficient (15–29 ng/mL), and severely deficient (<15 ng/mL). Prevalence rates of hypertension and odds ratios were calculated for each 25‐hydroxyvitamin D quartile, adjusting for age, sex, race, and renal insufficiency. A total of 2722 individuals met the inclusion criteria for the study. The overall prevalence of hypertension in the study population was 24%. Hypertension rates were 52%, 41%, 27%, and 20% in 25‐hydroxyvitamin D quartiles <15 ng/mL, 15 to 29 ng/mL, 30 to 39 ng/mL, and ≥40 ng/mL, respectively (P<.001). Odds ratios (95% confidence intervals) for hypertension adjusting for age, sex, race, and renal insufficiency were 2.7 (1.4–5.2), 2.0 (1.5–2.6), and 1.3 (1.2–1.6) for 25‐hydroxyvitamin D levels <15 ng/mL, 15 to 29 ng/mL, and 30 to 39 ng/mL, respectively, compared with the ≥40 ng/mL group. This study demonstrates increased rates of hypertension in individuals who tested for lower levels of 25‐hydroxyvitamin D starting at levels <40 ng/mL. This retrospective analysis raises the question of whether supplementing to optimal vitamin D levels can prevent or improve hypertension. J Clin Hypertens (Greenwich). 2011;13:170–177.

Vitamin D supplementation and recombinant human erythropoietin utilization in vitamin D-deficient hemodialysis patients.

INTRODUCTION We sought to examine the impact of ergocalciferol (ERGO) on recombinant human erythropoietin (EPO) use in a cohort of 25-OH vitamin D (25-D)-deficient hemodialysis (HD) patients. METHODS Baseline 25-D levels were obtained for all patients who received HD >6 months in our unit. Patients with levels between 10 and 30 ng/mL received ERGO 50,000 IU x 4 doses and patients with levels <10 ng/mL received 50,000 IU x 6 doses over a 4-month period. Monthly dose of EPO was recorded at baseline and after ERGO supplementation. RESULTS Baseline 25-D levels were <30 ng/mL in 89% of tested patients. Eighty-one patients were included in this study. Mean baseline 25-D level was 15.3 ± 7.1 ng/mL and increased to 28.5 ± 8.6 ng/mL after ERGO (p<0.0001), and median baseline EPO dose was 21,933 U/month (interquartile range [IQR] 13,867-35,967) and decreased to 18,400 U/month (IQR 11,050-33,000) after ERGO (p=0.17). Forty-six patients (57%) required less EPO after ERGO compared with baseline: 15,450 U/month (IQR 10,056-23,575) vs. 26,242 U/month (IQR 15,717-40,167), respectively (p<0.0001). Thirty-five patients (43%) required a higher dose of EPO after ERGO, 26,350 U/month (IQR 15,875-46,075) vs. 17,667 U/month (IQR 12,021-23,392), respectively (p=0.016). Mean age, sex, vintage, diabetes status, race and 25-D levels did not differ in these 2 groups of patients, either at baseline or after ERGO. Monthly hemoglobin, iron saturation, albumin, intact parathyroid hormone, calcium and phosphorus were unchanged after ERGO in these 2 groups. CONCLUSIONS ERGO use in 25-D-deficient HD patients may lessen the need for EPO. We recommend more aggressive supplementation with ERGO in future studies to achieve levels >30 ng/mL.

Comparison of Outcomes of Peritoneal Dialysis Catheters Placed by the Fluoroscopically Guided Percutaneous Method versus Directly Visualized Surgical Method

PURPOSE To compare complications in catheters placed by the fluoroscopically guided percutaneous method versus directly visualized surgery. MATERIALS AND METHODS A retrospective cohort analysis was performed. Mechanical complication rate data, including catheter leakage, malfunction, malposition, and bleeding, were compared between the two groups over a 1-year follow-up period. Additionally, exit site infection rates, tunnel infection rates, and peritonitis episodes were evaluated based on the incidence within 30 days of insertion and 30 days to 1 year after insertion. RESULTS A total of 101 patients were analyzed (52 in the fluoroscopic guidance group, 49 in the direct visualization group). Prevalence of diabetes was similar: 56% in the directly visualized surgery group and 47% in the fluoroscopically guided treatment group (P = .37). Although the difference was not significant, complication rates tended to be higher in the directly visualized surgery group compared with the percutaneous placement group. These included catheter leakage (13% vs 4%; P = .093), malfunction (11% vs 9%; P = .73), malposition (13% vs 6%; P = .20), and bleeding (8% vs 2%; P = .21). There were no differences in early and late exit site infections and tunnel infections. Late peritonitis rates were lower in the percutaneous placement group (20%) than in the direct visualization group (42%) (P = .018). Diabetic patients had approximately six times greater risk of catheter malfunction than nondiabetic patients regardless of method of catheter insertion. CONCLUSIONS Placement of peritoneal dialysis catheters percutaneously with fluoroscopic guidance is as safe as placement with direct visualization techniques.

Hyponatremia-what is cerebral salt wasting?

BACKGROUND Hyponatremia is a common electrolyte imbalance in hospitalized patients. It is associated with significant morbidity and mortality, especially if the underlying cause is incorrectly diagnosed and not treated appropriately. Often, the hospitalist is faced with a clinical dilemma when a patient presents with hyponatremia of an unclear etiology and with uncertain volume status. Syndrome of inappropriate antidiuretic hormone (SIADH) is frequently diagnosed in this clinical setting, but cerebral salt wasting (CSW) is an important diagnosis to consider. OBJECTIVE We wanted to describe the diagnosis, treatment, and history of CSW to provide clinicians with a better understanding of the differential diagnosis for hyponatremia. CONCLUSION CSW is a process of extracellular volume depletion due to a tubular defect in sodium transport. Two postulated mechanisms for CSW are the excess secretion of natriuretic peptides and the loss of sympathetic stimulation to the kidney. Making the distinction between CSW and SIADH is important because the treatment for the two conditions is very different.

Spontaneous retroperitoneal hemorrhage due to acquired cystic kidney disease

A patient with end‐stage renal disease on maintenance hemodialysis developed sudden severe abdominal pain and distension. He suffered a decline in his hematocrit and subsequent abdominal imaging revealed a large left‐sided retroperitoneal hemorrhage in the setting of atrophic, severely cystic kidneys. He underwent selective left renal artery angiography and embolization due to continued hemorrhage with stabilization in his condition. However, he became paraparetic within hours of the embolization procedure due to spinal cord infarct. Acquired cystic kidney disease is a very common entity in patients with chronic kidney disease. Complications include cystic hemorrhage or infection, erythrocytosis, and renal cell carcinoma. Screening of patients for cystic disease and malignant transformation remains a controversial topic; however, most advocate abdominal imaging after 3 to 5 years on dialysis.

Use of Phosphorus Binders among Non-Dialysis Chronic Kidney Disease Patients and Mortality Outcomes

Background: Whether the benefits of phosphorus binders extend to those without end stage renal disease is uncertain. Among a large diverse non-dialysis chronic kidney disease (CKD) population with hyperphosphatemia, we sought to evaluate phosphorus binder use and compare mortality risk between patients prescribed and not prescribed binders. Methods: A retrospective cohort study within an integrated health system (January 1, 1998 - December 31, 2012) among CKD patients (age ≥18) was performed. Non-dialysis CKD patients with 2 separate estimated glomerular filtrate rate (eGFR) <30 mL/min/1.73 m2 and serum phosphorus ≥5.0 mg/dL within 180 days of eGFR were included. Multivariable cox proportional hazards and inverse probability of treatment-weighted models were used to estimate mortality hazard ratios (HRs) for patients who received phosphorus binders compared to no binders. Results: Among 10,165 study patients, 2,733 subjects (27%) received phosphorus binders. Compared to the no-phosphorus-binder group, the binder group had mortality HRs (95% CI) of 0.86 (0.79-0.94) and 0.86 (0.80-0.93) using traditional multivariable and inverse probability of treatment-weighted models respectively. Sensitivity analyses removing patients who were prescribed binders >180 days after index date revealed no difference in mortality between those with binders and with no binders. Conclusion: Our findings from a real-world clinical environment revealed that 27% of hyperphosphatemic non-dialysis CKD patients were prescribed binders. They also had lower risk of mortality compared to those not prescribed phosphorus binders. However, the lower mortality risk was not observed when we accounted for immortal time bias. Whether phosphorus binder use in CKD improves survival remains to be determined.

Systemic mastocytosis presenting with acute oliguric renal failure: report of a case and review of the literature

A 61-year old African-American woman presented with abdominal pain, tender splenomegaly, anemia, and renal insufficiency. Bone marrow biopsy demonstrated systemic mastocytosis. She was treated with mediator-specific therapy and imatinib, but her renal and hepatic function deteriorated and she required maintenance hemodialysis. Renal biopsy demonstrated interstitial infiltration with mast cells and acute tubular necrosis. Acute kidney injury in the setting of systemic mastocytosis and imatinib therapy is discussed.

Hyponatremia in a patient with cryptococcal meningitis: Syndrome of inappropriate antidiuretic hormone (SIADH) or cerebral salt wasting (CSW)?

An 83-year-old man admitted for weakness, lethargy, and mental status changes was found to have human immunodeficiency virus (HIV) disease and cryptococcal meningitis. His hospital course was complicated by worsening hyponatremia (sodium < 136 mEq/L). By hospital day 6, the patient’s serum sodium had declined to 127 mEq/L from his admission level of 133 mEq/L. The initial impression was that the patient had syndrome of inappropriate antidiuretic hormone (SIADH) and fluid restriction to less than 1500 mL per day was initiated. By hospital day 11, serum sodium continued to decline, to 123 mEq/L, despite fluid restriction. The past medical history was remarkable for coronary artery disease, hypertension, hyperlipidemia, and anemia, but by self-report he had not been taking any medications. His review of systems was positive for intermittent bouts of diarrhea. Vital signs on day 11 included a temperature of 37.3 C, blood pressure (BP) of 105/55 mm Hg, and pulse of 90 beats per minute. The BP on admission had been 145/86 mm Hg but had steadily declined with fluid restriction. On physical examination, he appeared thin and cachetic with no evidence of jugular venous distention, rales, or peripheral edema to suggest volume overload. He had been receiving 2 to 4 L of isotonic saline daily for 5 days before the fluid restriction was initiated. The urine output continuously exceeded his intake by at least 500 mL per day throughout his hospital course. His only inpatient medications were amphotericin B and flucytosine. For nutritional supplementation, he was receiving a high-calorie supplement with free-water flushes via a nasogastric tube. Laboratory results revealed a serum sodium concentration of 123 mEq/L, serum potassium of 4.4 mEq/L, serum creatinine of 0.6 mg/dL, urine sodium of 139 mEq/L, serum osmolality of 272 mOsm/kg, and urine osmolality of 598 mOsm/kg (see Table 1). Urinalysis revealed a specific gravity of 1.030. A random serum cortisol level was 11.1 lg/dL. A thyroid-stimulating hormone (TSH) level was 1.32 lIU/mL. Brain natriuretic peptide (BNP) was elevated, at 686 pg/mL. A fractional excretion of uric acid was also elevated, at 83.8%. The clinical assessment was volume depletion given the high urine specific gravity, decreasing BP, and a negative fluid balance. The hyponatremia was determined to be due to sodium loss rather than dilution from inappropriate antidiuretic hormone secretion. Intravenous fluid (IVF) hydration with isotonic saline was initiated with a goal to keep the patient in positive fluid balance. The serum sodium level gradually improved to 140 mEq/L over the next 10 days. Attempts to decrease the rate of IVF resulted in a fall in serum sodium and improved when isotonic saline was increased. Eventually, the patient was placed on fludrocortisone, which normalized his urine output and serum sodium. The response to the treatment regimen supported our diagnosis of cerebral salt wasting (CSW). The patient’s serum sodium concentration upon discharge was 135 mEq/L.