Spontaneous massive bilateral peri-renal hemorrhage as a complication of ANCA-negative granulomatous vasculitis.

Spontaneous retroperitoneal hemorrhage (SRH) is a rare, life-threatening clinical entity most commonly associated with renal cell cancers. Systemic vasculitis has also been described as a rare cause of SRH. The current report describes a patient with acute kidney failure complicated by massive SRH, which occurred in the setting of anti-neutrophil cytoplasmic antibody (ANCA)-negative systemic necrotizing angiocentric granulomatous vasculitis involving multiple organs with minimal constitutional symptoms and no respiratory tract involvement.

Renal function recovery in dialysis dependent patients.

BACKGROUND: Recovery of renal function in patients requiring chronic dialysis is an uncommon phenomenon. It is important to identify these patients to avoid unnecessary, complicated and expensive dialysis. There are no recognized indicators that actually suggest such revival of renal function. The aim of the study is to evaluate the indicators of renal recovery in dialysis patients. METHODS: It is a retrospective chart review of 299 patients who initiated chronic hemodialysis from January 2005 to June 2008. Ninety-eight patients were included in the study. Exact logistic regression analysis was used to determine the predictors of renal recovery. RESULTS: Ten patients (3%) recovered their renal function. All of these patients had an episode of acute deterioration of renal function. Renal recovery correlated negatively with baseline serum albumin level (r=-0.53, P=<0.0001, age (r=-0.27, P=0.0054) and presence of hypertension (r=-0.30, P=0.0021) and DM (r=-0.30, P=0.0023) and positively with presence of human immunodeficiency virus infection (r=0.23, P=0.02). In multivariable exact logistic regression, analysis of low serum albumin level (exact odds ratio [OR] 27.09, P= 0.0008) and absence of DM (exact OR, 0.048, P=0.0002) were found to be the significant predictors of renal recovery. CONCLUSION: It is important to be aware of the possibility of renal function recovery in chronic dialysis patients, especially in patients who are not diabetic, have episodes of acute renal failure, and started on dialysis with low serum albumin level.

Assessment of 24,25(OH)2D levels does not support FGF23-mediated catabolism of vitamin D metabolites.

Progressive elevations of fibroblastic growth factor 23 (FGF23) in chronic kidney disease may reduce serum 25-hydroxyvitamin D (25(OH)) and 1,25-dihydroxyvitamin D (1,25(OH)(2)D) levels, via stimulation of 24-hydroxylase (Cyp24a1)-mediated catabolism of these vitamin D metabolites. To test this possibility, we measured serum concentrations of 24,25-dihydroxyvitamin D (24,25(OH)(2)D), a product of Cyp24a1 hydroxylation of 25(OH)D, in the Col4a3 knockout mouse, a model of Alport syndrome-derived chronic kidney disease, and in patients with chronic kidney disease of variable severity. There was an inverse correlation between serum FGF23 and both 25(OH)D and 1,25(OH)(2)D in the mouse model, but no significant relationship was observed in the cross-sectional patient cohort. The FGF23-dependent increase in Cyp24a1 mRNA expression in the mouse kidneys was consistent with the possibility that FGF23 induces vitamin D catabolism. There was, however, a reduction in serum 24,25(OH)(2)D levels, rather than the expected elevation, in both the mice and patients with chronic kidney disease. Low 25(OH)D and elevated FGF23 and parathyroid hormone levels were correlated with the reduced serum 24,25(OH)(2)D concentrations of these patients. Thus, we failed to find support for FGF23-mediated catabolism of vitamin D metabolites in chronic kidney disease assessed by 24,25(OH)(2)D levels.

Endovascular stent migration to the right ventricle causing myocardial injury.

Central stenosis of the subclavian and internal jugular veins is common in end stage renal disease. Treatment of these stenoses is difficult as these veins respond poorly to angioplasty alone and often require metallic stents to ensure patency. These stents are not without complications. Reports of stent fracture, thrombosis and vessel rupture abound in the literature. Stent migration can occur when used in large central veins leading to severe consequences such as pulmonary infarction, tricuspid regurgitation and right sided heart failure. In this report, we report a case of a subclavian vein stent which migrated into the right heart and caused subendocardial injury. As the use of vascular stents is becoming a common treatment option for central venous stenosis, the occurrences of serious complications associated with the stents are likely to rise.

Renal disease in AIDS: it is not always HIVAN.

Human immunodeficiency virus (HIV) infection can cause a broad spectrum of clinical manifestations, ranging from an asymptomatic carrier state to severe immunodeficiency. The most common renal lesion, HIV-associated nephropathy (HIVAN), is a sclerosing glomerulopathy. However, potentially reversible causes of renal disease in HIV-infected patients should also be considered. We describe two cases of patients with acquired immune-deficiency syndrome (AIDS) who presented with rapidly progressive renal failure but were found to have reversible etiologies. The first case was found to have syphilis and the second, disseminated histoplasmosis; their renal injury resolved after initiation of a third-generation cephalosporin antibiotic and amphotericin B, respectively.

Lactic acidosis in restrained cocaine intoxicated patients.

Severe lactic acidosis has been reported in patients struggling against restraints, especially in association with the use of stimulant drugs, such as cocaine. Profound acidosis occurring under these conditions can lead to cardiac arrhythmias, autonomic instability and cardiac arrest, a syndrome known as restraint associated asphyxia. Early recognition of this condition and removing the stimulus for lactic acid production (excessive muscle activity) by aggressive sedation and ventilatory assistance, coupled with fluid administration to improve tissue perfusion and lactate metabolism, can be life-saving. The current report describes a case of restraint associated severe lactic acidosis in a cocaine intoxicated patient that was successfully treated by sedation, muscular paralysis and mechanical ventilation. Public safety personnel must be aware of this potentially life threatening complication. Avoiding hobble and prone restraint positions may eliminate some of the problems that contribute to the pathophysiology of this condition.

Effect of α -Lipoic Acid on Oxidative Stress in End-Stage Renal Disease Patients Receiving Intravenous Iron.

Oxidative stress is associated with increased risk of cardiovascular disease in end-stage renal disease (ESRD) patients. Intravenous (IV) iron has been shown to increase oxidative stress. The aim of the study was to evaluate changes in oxidative stress markers following administration of IV sodium ferric gluconate (SFG) to ESRD patients with and without administration of the antioxidant, α -lipoic acid. This is an open-label, crossover study. 125 mg of IV SFG was administered during control (C) and intervention (I) visits. During the I visit, 600 mg of α -lipoic acid was given orally prior to IV SFG. Blood samples were collected at defined time periods for F2-isoprostane (FIP), lipid hydroperoxide (LHP), malondialdehyde (MDA), and iron indices. We recruited ten African-American ESRD subjects: 50% male; mean age 45 ± 9 years; mean hemoglobin 13 ± 1 g/dL; ferritin 449 ± 145 ng/mL; transferrin saturation 27 ± 4%. There were no significant differences in iron indices between the two visits after IV SFG. MDA, FIP, and LHP increased significantly for both C and I visits with a greater increase in the I group. Administration of IV SFG results in an acute rise in oxidative stress in ESRD patients. In contrast to previous studies, administration of α -lipoic acid was associated with a greater increase in oxidative stress.

C20209T prothrombin gene mutation associated deep venous thrombosis in a hemodialysis patient.

Venous thromboembolism (VTE) represents the formation of a blood clot in one of the deep veins of human body. The significant morbidity and mortality rates associated with VTE have spurred increasing investigations seeking to identify causative factors for this complex condition. While the most frequent causes of an inherited hypercoagulable state are the Factor V Leiden mutation and the prothrombin gene mutation, polymerase chain reaction (PCR) analysis has helped to identify other rare causes of inherited VTE. We report a case of a recurrent deep venous thrombosis in an end-stage renal disease patient. All laboratory tests for hypercoagulable states were normal. However, PCR analysis detected a rare polymorphism of prothrombin gene mutation at position C20209T, instead of G20210A. The patient was treated successfully with a high dose of warfarin to maintain adequate anti-coagulation during the 2-year follow-up.

Activation of FGF-23 mediated vitamin D degradative pathways by cholecalciferol.

CONTEXT: The optimal circulating concentration of 25(OH) vitamin D is controversial. OBJECTIVE: The aim was to investigate if FGF-23 and 24,25(OH)2D can guide cholecalciferol replacement. DESIGN: Oral cholecalciferol (10,000 IU weekly) administered to subjects with 25(OH)D levels < 20 ηg/mL and eGFR > 60 mL/min/1.73 m(2) (n = 25), chronic kidney disease (CKD) (n = 27), or end stage renal disease (ESRD) (n = 14). SETTING: The study was conducted at the Veterans Affairs clinics. MAIN OUTCOME MEASURE: Serum FGF-23, PTH, 25(OH)D, 1,25(OH)2D, 24,25(OH)2D, calcium, and phosphorous concentrations, and urinary excretion of calcium and phosphorus at baseline and after 8 weeks of treatment. RESULTS: Cholecalciferol treatment increased concentrations of serum 25(OH)D by (19.3 ± 8 ηg/mL, P = .001; 12.2 ± 9 ηg/mL, P = .0001) and 24,25(OH)2D (1.14 ± 0.89 ηg/mL, P = .0024; 1.0 ± 0.72 ηg/mL P = .0002), and reduced serum PTH (-11 ± 21 pg/mL, P = .0292; -42 ± 68 pg/mL, P = .0494) in normal and CKD subjects, respectively. Cholecalciferol increased serum FGF-23 levels only in normal subjects (44 ± 57 ηg/mL, P = .01). Increments in serum 25(OH)D positively correlated with serum FGF-23 and 24,25(OH)2D and negatively correlated with PTH. In ESRD, cholecalciferol administration increased 25(OH)D by (16.6 ± 6.6 ηg/mL P ≤ .05) without changing 24,25(OH)2D, FGF-23 or PTH levels. CONCLUSION: Modest elevations of serum 25(OH)D levels after cholecalciferol treatment are sufficient to induce compensatory degradative pathways in patients with sufficient renal reserves, suggesting that optimal circulating 25(OH)D levels are approximately 20 ηg/mL. In addition, catabolism of 25(OH)D may also contribute to the low circulating vitamin D levels in CKD, since elevations of FGF-23 in CKD are associated with increased 24,25(OH)2D after cholecalciferol administration.

Chronic kidney disease and diabetes mellitus predict resistance to vitamin D replacement therapy.

BACKGROUND: 25-Hydroxyvitamin D [25(OH)D] is a marker of nutritional status; however, chronic kidney disease (CKD) results in alterations in vitamin D metabolism, including the loss of vitamin D-binding proteins and alterations in CYP27B1 and CYP24 enzymes that metabolize 25(OH)D. This study was designed to determine the predictors of responsiveness to correction of vitamin D deficiency with oral vitamin D2 (ergocalciferol) in adults. METHODS: A retrospective study of 183 veterans with 25(OH)D level <30 ng/mL, who were treated with 50,000 IU per week of vitamin D2, was performed. Logistic regression models were developed to determine the factors predicting the response to treatment, defined as either the change in serum 25(OH)D level/1000 IU of vitamin D2 or the number of vitamin D2 doses (50,000 IU per dose) administered. RESULTS: The mean age of the patients was 63 ± 12 years. About 87% were men and 51% diabetic, and 29% had an estimated glomerular filtration rate of <60 mL/min/1.73 m. The average number of vitamin D2 doses was 10.91 ± 5.95; the average increase in 25(OH)D level was 18 ± 10.80 ng/mL. 25(OH)D levels remained <30 ng/mL in 61 patients after treatment. A low estimated glomerular filtration rate and the presence of diabetes mellitus were significant independent predictors for inadequate response to vitamin D2 treatment in logistic regression models. Patients with CKD required greater amounts of vitamin D2 to achieve similar increases in 25(OH)D levels, versus non-CKD patients. CONCLUSIONS: The presence of CKD and diabetes mellitus is associated with resistance to correction of 25(OH)D deficiency with vitamin D2 therapy. The underlying mechanism needs to be evaluated in prospective studies.

Severe hypernatremia correction rate and mortality in hospitalized patients.

INTRODUCTION: Hypernatremia is a common problem in hospitalized patients and is associated with high morbidity and mortality. This study was designed to evaluate whether physicians follow the recommended guidelines for the rate of correction of hypernatremia of ≤0.5 mEq/L/hr and to evaluate the effect of the rate of correction of severe hypernatremia on the mortality of hospitalized patients. METHODS: A retrospective chart review of 131 consecutively hospitalized patients with severe hypernatremia (serum sodium ≥155 mEq/L) was performed. Primary outcomes were 30-day patient mortality and 72-hour hypernatremia correction. The first 24-hour serum sodium (Na(+)) correction rate was tested as a categorical variable; slow rate (<0.25 mEq/L/hr) and fast rate (≥0.25 mEq/L/hr). RESULTS: The mean admission serum Na level was 159 ± 3 mEq/L. Ninety percent of patients received the recommended <0.5 mEq/L/hr serum Na(+) correction rate; however, hypernatremia was corrected only in 27% of patients after 72 hours of treatment. Thirty-day patient mortality rate was 37%. In multivariable analysis, do not resuscitate status [hazards ratio (HR), 3.85; P < 0.0001], slower correction rate of hypernatremia (HR, 2.63; P = 0.02) and high heart rate (>100 beats/min; HR, 1.99; P = 0.03) were the independent predictors of 30-day mortality. CONCLUSION: In patients with severe hypernatremia, the rate of correction of hypernatremia was slow and resulted in inadequate correction in majority of the patients. Both slow rate of hypernatremia correction during the first 24 hours and do not resuscitate status were found to be significant predictors of 30-day patient mortality.