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Patients with clinical and/or pathologic features of Alport disease or with unavailable abdominal imaging were excluded. The median ages at the onset, at the genetic diagnosis, and at the last follow-up were 0. The renal image studies revealed multiple renal cysts in 93% patients, renal parenchymal hyperchogenecity in 79%, and unilateral/bilateral renal hypoplasia in 50%. The other renal or extra-renal phenotypes included hyperuricemia in 79% patients and hypokalemia in 57%. The score at the last follow-up in ten patients except for 4 patients with transplantation was highest in patients with missense mutations (22. Hypokalemia was most common in patients with total deletion mutations (83%) and least common in those with missense mutations (0%, P=0. Of the 11, 3 were reported to have glomerular disease, 1 had haematuria, 1 had a renal transplant, and 6 had diabetes (55% vs. Review of magnetic resonance imaging and ultrasound going back to 2003 showed normal sized kidneys and presence of more than 4 cysts in each kidney, some of which were mildly complex. Chronic symptomatic hypomagnesemia was present since at least 2015 with serum magnesium ranging from 1. Fractional excretion of magnesium was 29%, consistent with renal magnesium wasting. Intact parathyroid hormone ranged from 83-112 pg/mL but serum calcium, phosphorus, 25 dihydroxyvitamin D were normal. She was started on amiloride and slow release magnesium supplementation with near normalization of her serum magnesium. De novo mutations occur in up to half of patients leading to diagnosis later in life. Additionally, these patients should be monitored for progressive kidney disease and undergo periodic screening for renal cell carcinoma. Department of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Descriptive analyses were conducted on the following baseline measures: demographics, comorbidities, and disease characteristics. Additional analyses evaluating the real-life impact of tolvaptan on clinical outcomes, healthcare utilization, and quality of life are needed. Treatment discontinuation rates at 12, 24 and 36 months were 14%, 21% and 26%, respectively. Descriptive analyses provided baseline patient characteristics and follow-up measures on a subset of patients eligible for treatment pattern assessment. Based on the data currently available, most patients were between 35-55 years, equally male or female, and were non-Hispanic or non-Latino whites. The patients included in the treatment pattern analysis remained on tolvaptan close to 1 year. Funding: Commercial Support - Otsuka Pharmaceutical Development & Commercialization Inc. Additional studies assessing real-world evidence supporting tolvaptan treatment in this population are needed. Funding: Commercial Support - Otsuka Pharmaceuticals Development & Commercialization, Inc. Unadjusted and multivariable mixed-effects linear regression models, adjusted for age, sex, body mass index, estimated glomerular filtration rate, net acid excretion and height-adjusted total kidney volume were used to assess the association of Tolvaptan with urinary parameters relevant for kidney stone formation. Results: 125 participants (38 with and 87 without Tolvaptan treatment) were included in the analysis. In multivariable analysis, Tolvaptan treatment was associated (adjusted estimate of the difference Tolvaptan vs. In addition, Tolvaptan treatment was associated with decreased net acid excretion in mEq/mmol creatinine per day (-0.
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Do not be misguided by guidelines: the calcium x phosphate product can be a Trojan horse. Dietary intake of phosphorus modulates the circadian rhythm in serum concentration of phosphorus. Evidence that postprandial reduction of renal calcium reabsorption mediates hypercalciuria of patients with calcium nephrolithiasis. Lack of significant circadian and postprandial variation in phosphate levels in subjects receiving chronic hemodialysis therapy. Parathyroid hormone assays evolution and revolutions in the care of dialysis patients. Parathyroid hormone 7-84 induces hypocalcemia and inhibits the parathyroid hormone 1-84 secretory response to hypocalcemia in rats with intact parathyroid glands. Improved radioimmunoassay for vitamin D and its use in assessing vitamin D status. Determination of 25-hydroxyvitamin D in human plasma using high-performance liquid chromatography tandem mass spectrometry. Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D. Patients with prior fractures have an increased risk of future fractures: a summary of the literature and statistical synthesis. The effect of alendronate therapy on osteoporotic fracture in the vertebral fracture arm of the Fracture Intervention Trial. The association of radiographically detected vertebral fractures with back pain and function: a prospective study. Increased incidence of hip fractures in dialysis patients with low serum parathyroid hormone. Increased risk of mortality associated with hip fracture in the dialysis population. Spectrum of renal osteodystrophy in children on continuous ambulatory peritoneal dialysis. Effect of alfacalcidol on natural course of renal bone disease in mild to moderate renal failure. Evolution of bone and plasma concentration of lanthanum in dialysis patients before, during 1 year of treatment with lanthanum carbonate and after 2 years of follow-up. Low vs standard calcium dialysate in peritoneal dialysis: differences in treatment, biochemistry and bone histomorphometry. Low dose calcitriol versus placebo in patients with predialysis chronic renal failure. Improvements in renal osteodystrophy in patients treated with lanthanum carbonate for two years. Effects of sevelamer hydrochloride and calcium carbonate on renal osteodystrophy in hemodialysis patients. Adynamic bone disease with negative aluminium staining in predialysis patients: prevalence and evolution after maintenance dialysis. Spectrum of renal bone disease in end-stage renal failure patients not yet on dialysis. Renal osteodystrophy in Ramathibodi Hospital: histomorphometry and clinical correlation. Renal bone disease in 76 patients with varying degrees of predialysis chronic renal failure: a cross-sectional study. Fractures and vertebral bone mineral density in patients with renal osteodystrophy. Correlation of bone mineral density with the histological findings of renal osteodystrophy in patients on hemodialysis. Coronary calcification in hemodialysis patients: the contribution of traditional and uremia-related risk factors.
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Families often are concerned about whether to re-dose antiseizure medications with emesis; we advise our parents to repeat the dose if vomiting occurred less than 30 minutes from dose administration. Some children require slower delivery of feeds, either with more frequent, smaller meals or, if gastrostomy tube fed, with slower rates of infusion with a feeding pump. For short-term vomiting around times of illness, use of Powerade Zero or Propel Zero can provide hydration and electrolytes, without carbohydrates. In instances of more prolonged feeding intolerance, half strength Pedialyte to provide a source of calories is usually well tolerated, without significant reduction in ketosis. Practitioners should be aware of medications that could worsen acidosis, especially common antiseizure medications, such as topiramate and zonisamide. In some cases, it may be necessary to decrease these medications in order to manage acidosis. During initiation, acidosis should be treated with aggressive hydration and use of oral alkalinizing agents. Once the patient is on a stable diet ratio, with adequate doses of alkalinizing agents, acidosis becomes less problematic. However, during times of illness, with decreased oral intake and/ or vomiting, acidosis can again become problematic and typically can be managed with hydration. This can be particularly problematic in those who had preexisting constipation, and for those who have impaired mobility. Increased hydration may help with symptoms, but many patients will require medications to manage their constipation. Polyethylene glycol (Miralax) is a common choice for treatment as it is not significantly absorbed in the gut and is 68 68 section I: Ketogenic Diet for Epilepsy in the Clinic commonly, have gritty urine or pain. There may be a role for periodically checking serum uric acid and urinary calcium/creatinine ratios. Children with family histories of kidney stones receiving carbonic anhydrase inhibitors (topiramate, zonisamide, or acetazolamide) are also at higher risk for stones (Furth et al. Treatment includes fluid liberalization and urinary alkalization with bicarbonate (Sampath, 2007). In children with a higher risk for kidney stone formation, prophylactic treatment with Polycitra K has been shown to reduce the incidence of kidney stones in this susceptible population (McNally et al. If patients have severe hypoglycemia (<30 mg/dL) or symptomatic hypoglycemia (<40 mg/dL with lethargy, vomiting, diaphoresis, seizures, or shakiness), small amounts of juice (1020 mL) or dextrose (D5W infusion until blood glucose is >60 mg/dL) can be given to correct the blood sugar. If hypoglycemia is a persistent problem, a reduction in ratio should be considered. Once stable on the diet, glucose tends to be on the low end of normal (5070 mg/ dL), but is overall very stable. However, there have been reports of development of urolithiasis after just 1 month on the diet. The majority of stones are uric acid stones, however, calcium oxalate, calcium phosphate, and mixed calcium/uric acid stones are seen. This can be compounded by fluid restriction, which produces a more acidic urine and decreased urine flow, with precipitation of urate crystals. Urinary citrate is an inhibitor of calcium crystal formation; therefore, low urinary levels increase the risk of calcium stone formation. Children typically present with gross or microscopic hematuria, therefore patients require regular screening urinalysis. These effects were reversible, with resolution when the diet was discontinued (Woody et al. Other conditions associated with ketosis, such as diabetes mellitus, alcoholism, glycogen storage disease, protein-calorie malnutrition, certain carbohydrate-restricted diets, and intralipid infusions, have also reported impairments in neutrophil function. The exact mechanism is not well understood but is likely related to serum metabolites that affect early processes in phagocytosis (Woody et al. In the study, some did suggest additional supplementation may be needed for zinc, magnesium, selenium, and phosphorous, but this was not a universal recommendation, and may be considered on an asneeded basis depending on laboratory values. Vitamin levels should be followed on a routine basis during follow-up, and early supplementation to avoid deficiencies is optimal.
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Adjustment for Hb only slightly attenuated the effects, and the results were similar for subgroups of patients with Hb <11. Plasma and urine ferritin were measured at baseline, then 2 h (plasma) or 24 h (urine) through 168 h post-treatment to assess clinical response. Dose-dependent increases in plasma ferritin were observed in all subjects within 2 h of treatment and reached statistical significance by 8-12 h. This is the first report of ferritin level increases within only 2 h by an iron formulation. Reducing the frequency of repeat infusion benefits healthcare resource & patient acceptance. These data may predict a future dosing strategy that is more likely to meet iron requirements in a single, or at least a minimum number of infusions. The cumulative amount of iron to attain and maintain a target Hb >100g/L was determined. This gives an insight into how future approaches to iron dosing could be considered. Response to iron therapy was defined as improvement in both hemoglobin and hematocrit after iron therapy. Changes of serum iron were used as a surrogate measure of adherence to iron therapy. Iron therapy resulted in a significant increase in transferrin saturation (14 to 21%, p<0. Non-responders had a significantly smaller change in serum iron after iron therapy compared to responders (3 vs. Baseline body weight and height Z scores were significantly lower in non-responders than in responders (-0. Response to iron therapy may be related to medication adherence and baseline nutritional characteristics of study participants. Multiple-choice knowledge and self-efficacy confidence questions were presented both before and immediately after each activity. A repeated pairs pre-/post-assessment study design was used and chi-square test (5% significance level, P <. The activity launched June 20, 2019 and data were collected through July 11, 2019. Overall improvements were seen for both activities after participation: Activity 1: N=75, P<. Three multiple-choice knowledge/ competence questions and 1 self-efficacy confidence question were presented both before and immediately after each activity. The activity launched June 27, 2019 and data were collected through August 27, 2019. Results: In total, 62 nephrologists answered all pre-/post-assessment questions and were included in the study. Physicians completed an online survey providing information on their demographics, opinions on the diagnosis and treatment of anemia, and the current unmet needs they believe exist in the management and treatment of anemia. For the last 3 weeks of the diets, the mice were treated with vadadustat (75 mg/kg/day via oral gavage) or vehicle solution. Vadadustat treatment was also associated with improved kidney function (Fig 1b) and decreased expression of renal fibrosis markers. Survey participants were contacted 8 weeks later to assess self-reported actual changes in practice. Funding: Commercial Support - American Regent Poster Thursday Anemia and Iron Management Oxidative Stress and Heme Metabolism in Red Blood Cells of Hemodialysis Patients Gabriela F. Andrade,2 Nadja Grobe,1 Xia Tao,1 Roberto Pecoits-Filho,2,4 Peter Kotanko,1,3 Andrea N. The main comorbidities and risk factors in the subjects with anemia were type 2 diabetes mellitus and hypertension (55%), proteinuria (38%), hypoalbuminemia (34%), hyperkalemia (37%) overweight or obesity (58%), hyperglycemia (45%) hypertriglyceridemia (35%) and hypercholesterolemia (31%). The difference in mean Hgb values at Week 24 between treatment groups was summarized overall and by subgroup. Results of an ongoing, phase 3 dialysis study of daprodustat compared with conventional treatment are awaited to confirm these initial observations. Descriptive analyses were performed to assess betweentrial differences with respect to baseline Hb and Hb target ranges.
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Rouach and colleagues provided more direct evidence to show that electrical activities in neurons are regulated by the metabolic pathway from inhibitor (Garriga-Canut et al. The ketogenic diet has also been shown to suppress seizures in mice by increasing the activation of adenosine A1 receptors (Masino et al. Consistent with these findings, the direct activation of adenosine A1 receptors has been shown to suppress chronic seizures in a mouse model of mesial temporal lobe epilepsy (Gouder et al. These extensive studies have uncovered the mechanisms underlying the antiepileptic effects of the ketogenic diet. Since the ketogenic diet changes energy metabolites (glucose and ketone bodies), it is hypothesized that the brain has "metabolic pathways" that play key roles in the antiepileptic effects of the ketogenic diet. In other words, there are assumed to be "metabolic enzymes" that regulate electrical activities in neurons and suppress seizures in vivo in the same manner with the ketogenic diet. In order to explore these metabolic pathways and enzymes, we focused on the astrocyte-neuron lactate shuttle in the brain, because this lactate shuttle was known to be a metabolic pathway involved in the regulation of electrical activities in the brain (Rouach et al. The role of astrocytes (a type of glial cell) as the energy supplier to neurons has recently received increasing attention (Bйlanger et al. Glucose is directly transported into neurons, and then converted to pyruvate by glycolysis. Decreases in glucose and increases in ketone bodies are elicited by the ketogenic diet. By using this property, a group of nearby astrocytes can be controlled by selective filling of active small molecules into single astrocytes using patch pipettes (Rouach et al. Rouach and colleagues made filling of glucose into single astrocytes in hippocampal slices, and then examined the effects of the deprivation of extracellular glucose on hippocampal synaptic transmission. They demonstrated that, although glucose deprivation reduced synaptic transmission, these reductions were rescued by the selective filling of glucose into astrocytes (Rouach et al. Rouach and colleagues also showed that epileptiform activities in hippocampal slices were regulated by the selective filling of glucose into astrocytes (Rouach et al. The ketogenic diet is known to increase ketone bodies and decrease glucose in the body (Bough et al. Thus, the astrocyte-neuron lactate shuttle is likely to regulate membrane potentials in neurons. We also obtained direct evidence to show that membrane potentials in neurons are regulated by lactate released from astrocytes (Sada et al. In order to further confirm that this hyperpolarization in pyramidal cells was actually due to reductions in the release of lactate from astrocytes (see Figure 29. These in vitro studies revealed that the release of lactate from astrocytes to neurons regulates membrane potentials in neurons. We also obtained evidence to show that this lactate release is actually weakened by the ketogenic diet (Sada et al. Mice were fed a ketogenic diet for about 3 weeks, and the lactate concentration in the hippocampus was measured and compared with that in the hippocampus of age-matched mice fed a standard diet. The measurement of lactate concentration revealed that the hippocampal lactate was lower in mice fed the ketogenic diet than in those fed the standard diet (Figure 29. Thus, the release of lactate in this lactate shuttle is lowered by the ingestion of the ketogenic diet (Figure 29. Neurons are recorded in the whole-cell mode using normal intracellular solution, whereas astrocytes are recorded in the cell-attached mode using intracellular solution including oxamate. Thus, lactate is a mediator for this astrocyteinduced electrical regulation in neurons. Microinjection of kainic acid into the hippocampus is known to produce a mouse model of mesial temporal lobe epilepsy, which exhibits spontaneous paroxysmal discharges with abnormal morphology in the hippocampus (Riban et al. Lactate dehydrogenase as a metabolic target against epilepsy will be useful in the development of new antiepileptic drugs. Identification and activity of a series of azole-based compounds with lactate dehydrogenase-directed anti-malarial activity. Predominant enhancement of glucose uptake in astrocytes versus neurons during activation of the somatosensory cortex.
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Oligo-anuria at admission and leukocytosis is associated with poor outcomes during hospitalization. The administration of dextrose and saline containing iv fluids in the early presentation was associated with the decreased requirement of dialysis (p=0. Peak white blood cell count (Wbc) had a strong correlation with days of hospitalization (p<0. Early diagnosis and iv fluids before the onset of renal failure may help to prevent dialysis-related morbidity at the time of admission. In Group 1, 22/63 patients had or developed hemoglobinuria while the remaining 41/63 were and remained negative. Methods: this multicenter case series study was performed between 2010 and 2019 in Pediatric emergency departments and clinics belonging to a network of 63 pediatric hospitals in Northern Italy (referral population: 12 million general population; 2. We suggested that patients could be monitored for relapses, with hemoglobinuria (twice weekly and during intercurrent diseases) based on the hypotesis that a thrombotic microangiopathy involving the glomerulus, cannot take place without hematuria. Its management is entirely based on supportive care, which includes generous fluid infusions, since dehydrated patients have been described to have a worse outcome, compared to normoand overhydrated patients. Wijnsma,1 Marloes Michels,1 Roel Kurvers,7 Joanna Van Wijk,2 Antonia Bouts,2 Valentina Gracchi,3 Flore Horuz-Engels,7 Mandy G. Patient cohort studies including clinical features offer important data in rare renal diseases. Moreover, biomarkers are increasingly used to select patients for clinical trials with novel complement-targeted therapies. This retrospective study describes complement biomarker profiles and outcome of 29 Dutch children. Methods: Patients with a C3G diagnosis from 5 Dutch university medical centers (1992- 2014) were included. Specialized biochemical assays were used to detect complementdirected autoantibodies and complement biomarkers. Patients presented with proteinuria and hematuria (>90%) and low serum C3 levels (84%). No significant differences in clinical or laboratory features were observed between patients with and without a relapse and persistent renal sequelae. Conclusions: We present the extensive description of clinical, genetic, and biochemical complement features of a large pediatric C3G cohort. Methods: We used the Scientific Registry of Transplant Recipients to identify all patients who received a kidney transplant in the United States for Alport syndrome between 1987 and 2017. Results: Between 1987 and 2017, 4105 Alport patients received a kidney transplant in the United States. Pathological findings by Oxford classification showed significant differences in the frequency of M1 (94. Fluorescence findings showed significant difference in the frequency of fibrinogen deposition (93. Poster Thursday Pediatric Nephrology: Glomerular Disease and Transplantation Risk of Rituximab-Associated Severe Adverse Events Increases with Young Age in Children with Nephrotic Syndrome Camille Laroche,2 Dominique Lemieux,2 Anne-Laure Lapeyraque,2,1 Adrien Flahault. Severity of adverse events was graded according to the Common Terminology Criteria for Adverse Events. Demographics and clinical data among those seen by nephrology were compared to those not seen by nephrology. By the end of follow up, 26 (3%) had estimated glomerular filtration rate <60 mL/min/1. Four had normal female external genitalia, and 5 had various abnormalities of male genitalia. All progressed to end stage kidney disease at a median age of 5 years (1 month to 14 years). Of two pubertal males, one had hypogonadism, and both were monitored for gonadal tumor. Background: Pre-transplant evaluation is mandated by Centers for Medicare and Medicaid Services, but there is institutional variation in implementation. Our interview study aims to fill the knowledge gap about family experience of the evaluation for children. Methods: Interviews took place 07/2019 - 02/2020 with caregivers of children referred for kidney transplant at our center 07/2017 - 12/2018.
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Despite almost 100 years of clinical use, the mechanisms underlying the success of ketogenic diet therapy are not well understood. In recent decades, ketogenic diet has increasingly been noted as a useful therapy for medically refractory epilepsy (Hallbook et al. The patients of temporal lobe epilepsy are well known to be frequently resistant to antiepileptic drugs (Wiebe and Jette, 2012). As mentioned previously, the first choice of treatment for mesial temporal lobe epilepsy associated with hippocampal sclerosis is surgery (anterior temporal lobectomy or selective amygdalohippocampectomy) because of good therapeutic outcomes (Tanriverdi et al. For temporal lobe epilepsy patients who are not good candidates for surgery, however, ketogenic diet is one of the therapeutic options (Ray and Wyllie, 2005). Thus, a natural question is how the ketogenic diet produces its beneficial effects in temporal lobe epilepsy. There are two approaches for electrophysiological recordings of any brain region: in vivo and in vitro. In vivo electrophysiological recording of hippocampus is usually done by extracellular recording of electrically evoked activity (Stewart and Reid, 1993), or continuous recording of spontaneous field activity (Li et al. In vitro electrophysiological recording is done using single-cell intracellular sharp electrodes (Abe and Ogata, 1981) or patch-clamp electrodes (Kawamura et al. As compared with in vivo hippocampal recordings, the advantages of hippocampal slices are several-fold: (1) Ease of use: acute brain slices must be maintained by perfusion with oxygenated artificial cerebrospinal fluid (Sakmann et al. Thus, it is easy to apply and wash out several agonists and/ or antagonists of various proteins such as channels, receptors, and transporters, and it is easy to examine the detail of functional mechanisms of neuronal activities; (2) Reduction: we usually make 36 brain slices from one rodent and get 36 recordings from them, allowing us to reduce the number of animals used; (3) History: a huge number of electrophysiological experiments have been done using hippocampal slice preparations in the last half-century. Several methods for causing seizure-like bursting in vitro have been used in the hippocampal slice preparation, including kindling (Sayin et al. All these approaches support the use of hippocampal slice preparations to elucidate epileptic mechanisms. On the other hand, the pitfall of in vitro recording is that the environment of acute brain slice preparations is different from the in vivo condition. We make a slice by cutting brain tissue and that causes traumatic injury: reactive gliosis occurs in the acute hippocampal slice (Takano et al. Also, artificial cerebrospinal fluid does not exactly reproduce actual cerebrospinal fluid. Thus, results from in vitro hippocampal slice preparations should be confirmed by in vivo electrophysiological recordings or behavioral tests as much as possible. For that reason, both in vivo and in vitro electrophysiological recordings are useful, and both are essential for epilepsy research. In vivo recording clearly does not have this problem, because it uses the whole body of experimental animals and dietaltered metabolism is maintained (Koranda et al. Therefore, special strategies must be implemented for examining mechanisms of the ketogenic diet using hippocampal slice preparations; in this section, we review three of these approaches (Figure 21. Direct Application of Ketone Bodies the ketogenic diet was developed to mimic fasting, which alleviates epileptic seizures (Wilder, 1921). Ketogenic diet increases ketone bodies (-hydroxybutyrate, acetoacetate, acetone), synthesized from free fatty acids in the liver (Masino and Rho, 2012) and then used for energy in the brain instead of glucose (Masino et al. Therefore, one approach to reproducing a ketogenic diet in a hippocampal slice is direct application of ketone bodies, revealing whether ketone bodies modulate neuronal activity directly. In this paradigm, hippocampal slices are taken from control dietfed animals and dissolved ketone bodies are applied in an extracellular solution such as artificial cerebrospinal fluid (Figure 21. Extracellular glucose is reduced during incubation and recording to maintain the in vivo effect of the ketogenic diet. They made organotypic hippocampal slices, which were cultured with low glucose and 10 mM -hydroxybutyrate medium for at least 3 days. This chronic in vitro ketosis, however, did not alleviate intrinsic or induced epileptiform discharges (but was neuroprotective). All of these studies concluded that ketone bodies do not directly affect synaptic transmission in the rat hippocampus. In sum, several studies have used direct application of ketone bodies in hippocampal acute slices or organotypic cultures, and both positive and negative results have been found.
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Few studies have demonstrated immunohistochemically-proven hemoglobin casts on kidney biopsy associated with intravascular hemolysis. Below is a case of Rifampin-induced hemolysis associated hemoglobin cast nephropathy. A kidney biopsy was planned and hemodialysis was performed to optimize platelet function. Kidney biopsy demonstrated intratubular pigmented casts that were strongly positive for hemoglobin A immunohistochemical stain confirming the diagnosis of hemoglobin cast nephropathy [Figure 1]. Diagnosis is multifaceted requiring a clinical history, exam, lab workup and most importantly, a kidney biopsy. She was diagnosed with bladder perforation and underwent open bladder repair emergently. Discussion: Uroperitoneum can result in the reabsorption of urine into the systemic circulation, while sodium and chloride ions move in the opposite direction. Complex extraperitoneal and all intraperitoneal bladder injuries require surgical repair. This puzzling presentation was presumed to be driven by an unidentified viral illness. Understanding the mechanisms of injury is essential to develop targeted therapies. Samples were tested with liquid chromatography/tandem mass spectrometry with data-independent acquisition. Pathway enrichment analysis linked these proteins to cell cycle and ubiquitous pathways. Gynecological and colorectal surgeries are the most common surgeries associated with bladder injury. Clinical manifestations include gross or microscopic hematuria, ascites, and/or difficulty voiding. Introduction: Oxalate nephropathy is an uncommon and potentially devastating cause of acute kidney injury that can lead to end-stage kidney disease. Oxalate nephropathy can be hereditary (as in hereditary hyperoxaluria), related to toxins (such as ethylene glycol), medications, like high-dose vitamin C, or enteric malabsorption (such as gastric bypass surgery or malabsorptive disorders). Oxalate nephropathy occurs when calcium oxalate crystals form and deposit in the renal tubules and interstitium, leading to acute tubular necrosis. Case Description: A 71 year old female with a medical history of pancreatic adenocarcinoma s/p Whipple procedure seven months earlier and chronic kidney disease stage 3 (baseline creatinine 1. Initial evaluation was concerning for volume depletion, as she improved with intravenous fluids. Over the next several months, she had repeated hospital admissions with worsening nonoliguric renal failure that seemed to respond to intravenous fluids in the hospital but worsened at outpatient visits. Urinalysis repeatedly showed no microscopic hematuria and low-level proteinuria, and urine microscopy showed coarse granular casts, consistent with acute tubular necrosis. Kidney biopsy was consistent with acute tubular injury and extensive tubular calcium oxalate deposition concerning for oxalate nephropathy. Discussion: Oxalate nephropathy is a rare complication of pancreatic surgery and ascorbic acid use. In malabsorptive disorders, a higher concentration of fatty acids are present in the gastrointestinal tract, which bind calcium, leaving less to bind oxalate, and thus more oxalate is absorbed. High urinary oxalate can cause crystallization in tubules, leading to acute renal failure. Treatment is supportive, with removal of offending agents, oral calcium supplementation, and adequate oral hydration. Despite this, our patient progressed to end-stage renal disease requiring dialysis. A kidney biopsy was performed and showed patchy cortical atrophy and interstitial fibrosis with moderate vascular sclerosis and focal remodeling of the glomerular basement membranes consistent with prior vascular injury as well as acute tubular injury. A hematologic evaluation did not reveal an etiology and further history revealed use of sumatriptan 8-10 times per month. The biopsy findings of primarily vascular injury were initially felt to be cryptogenic, but further review revealed the etiology to most likely be triptan induced.
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Certainly analytical chemists could be of major assistance in the design of such instruments. Important instru- mental design considerations which must be kept in mind in oceanographic studies include not only corrosion and erosion effects of the ocean the ocean depths. Since the deepest known area in the ocean, the Mindanao Trench, has a reported depth of 37,782 feet, a pressure equivalent to well over 16,000 Ib-in"^ must be withstood. One published article was noted in which activation analysis was used to analyze the mineral content of the sea floor. The gamma rays produced by the irradiated sea floor indicated the elemental content. Kneip - I would like to make a few remarks concerning the concentra- tion of heavy, or transition, metals. Statements were made today and other days that the heavy metals this become concentrated. We learned that the pesticides are concentrated up through food chains to the point where the top predators are being lost because of this concentration effect. In fact mercury is an exception because we are dealing with a heavy metal which is converted to a metalorganic compound and it concentrates in the food chain because of the specific transfer of the organic material. There is a methylmercury-protein complex in muscles, in addition to storage like the pesticides in fat. Thus to use mercury as a representative example of heavy metal concentration factors in biological systems is misleading. The Institute of Environmental Medicine of New York University Medical Center has been specifically and rather intensely looking at manganese and cobalt in the Hudson River estuary in the vicinity of a nuclear plant because of interest in the circulation of radionuclides that are released by that plant. There is a need to predict what will happen to future releases by additional plants being built in the region. The very first thing one finds out is that these transition metals are heavily concentrated by plants, and this includes plankton and rooted plants. The higher forms of life in the region, the fish for instance, do not have nearly as high a con- Not only this, but response times are vastly different. These time periods have not been resolved but they are less than a week for rooted plants, while for the entire system, i. It was found that manganese and cobalt for in- anywhere from a month the sedimentary interactions have stance, regardless of their origin, transfer to the sediments while the water in the region is fresh, but when the salinity reintrudes into the area, huge into the water. They take it up, concentrations jump, and the whole system reverses itself when another intrusion of fresh water comes through the region. This is one of the confusion factors that adds to the fun in studies of the estuary. It is fascinating to contemplate what is happening to some of the other heavy metals. All of these materials seem to go to the sediments, but whether all of them will behave in a similar fashion is doubtful. The chemistry of manganese is unique, so one may find that there is a storehouse for some of the heavy metals in this region rather than simply a transfer point. It would be interesting to know whether manganese itself in undergoing this cycling is merely temporarily held in the region and is carried out to sea as it is redissolved. There are times and places when the team leader in these problems should be an analytical chemist. It is very obvious from some of the problems of understanding interactions of sampling, the sampling container, the need that originated the study, the analytical methods that are available, and finally the interpretation of the results to get back the answer to that original need, that the analytical man is the only one who is going to put it all together. He is able to take some of the information from one particular speciality and some from another, then supply the overall look at the whole problem and become the team leader. We ought to try to get into the heart of the problem and, where it is appropriate, take the lead. Profiles are seen that can only be interpreted by the bubbling of methane, motion of organisms, etc. So we are going to be stuck with the familiar problem of how to understand "turbulent diffusion" while looking at the flux of these metals from the sediments. In reference to the comment this morning about phosphate, a lot of phosphate is seen in the sedimentary record.
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The early injury phase (<4hr) was defined by mild, but significantly increased plasma creatinine indicating promptly reduced renal function along with upregulated injury response genes. Induction of pro-apoptotic and pro-fibrotic genes occurred during the later phase, in line with exacerbated renal function. Funding: Commercial Support - Silver Creek Pharmaceuticals Publication-Only Misleading Serologies in Thrombotic Microangiopathy due to Malignant Hypertension Taqui Khaja,1 Rajeev Raghavan,1 William F. Introduction: Nephrologists use autoimmune panels to screen for glomerular disease. Some of these markers cause false positives in other systemic diseases which leads to misdiagnosis. She was re-admitted few weeks later with uremia and hypertensive urgency with pressures of 209/104. Her biopsy was significant for global glomerulosclerosis, glomerular ischemia, and severe interstitial fibrosis with tubular atrophy. There was extensive arteriolar onion skin intimal fibroplasia with red blood cell fragments. Her biopsy lacked findings of vasculitis due to an absence of necrotizing crescentic glomerulonephritis and negative immunofluorescent stains. The markers were correlated to intensity of the disease because the patients with active disease had higher tighters. This case also emphasizes the importance of kidney biopsy in order to distinguish between active vasculitis and non-vasculitic diseases. Introduction: Sarcoid is a multi-organ system disease primarily affecting the lungs. Sarcoidosis is a genetic associated autoimmune disease more prevalent in African Americans. Renal sarcoidosis manifests in about 5-20% of patients with hypercalcemia, hypercalciuria, and nephrocalinosis on normal screening. Renal parenchymal involvement is typically granulomatous tubulointerstitial nephritis. Neuro-sarcoid also occurs in about ј of patients, affecting primarily the cranial nerves. Case Description: 63-year-old white male with a history of rheumatoid arthritis, pulmonary nodules, glaucoma, presented with one year of blurry vision and weird psyche. He was referred to nephrology after an ophthalmologist found intermittent diplopia, transient optic disc swelling and intraretinal hemorrhage. Renal biopsy demonstrated noncaseating granulomatous interstitial nephritis, numerous noncaseating granulomas with giant cells. He was referred to Cleveland Clinic Sarcoid Clinic and started on 40mg prednisone for renal sarcoid. Discussion: Less than one in ten patients present solely with extrapulmonary sarcoid. This case demonstrates a rare presentation of neuro-ocular and renal sarcoidosis in the absence of lung findings. The hyperinflammatory response of the body, associated with oxidative stress is a key player in mechansim of multiple organ failure. Conclusions: In this experimental model that mimics human Covid 19 multiorgan failure, antiooxidant improved survival, lung and kidney injury and also oxidative stress in the kidney. Traditional pharmacotherapy includes phosphorus binders, Vitamin D analogues, and oral calcimimetics. Etelcalcetide is an intravenously delivered calcimimetic approved to treat hyperparathyroidism. A predictive algorithm could assist clinicians in assessing the potential effect of a given dose. Methods: We used tree ensemble (RandomForest) models for their ability to model the data non-linearities. Model inputs were historic data (calcimimetic dosing, labs, dialysis records, demographics, and phosphorus binder orders) and future calcimimetic dosing. In addition, for the 1-, 2-, and 3-month predictions, 71%, 65%, and 63% of the predictions, respectively, lie within ±0. Limitations include: a relatively small data set which precluded the use of other models.