Fractional Excretion Of Sodium Research Articles

#1925 A rare cause of hyponatremia due to adrenal insufficiency in a patient with small cell lung cancer

Abstract Background and Aims Hyponatremia is the most frequent electrolyte disorder. Small Cell Lung Cancer (SCLC) release often antidiuretic hormone paraneoplastically. But Adrenal insufficiency is a rare cause of hyponatremia in SCLC. Prior one can cause euvolemic hyponatremia, latter one can cause hypovolemic hyponatremia. Opposite treatments should be applied for each one. So They should be investigated carefully before starting the treatment. Method A male patient who had metastatic SCLC was admitted to the emergency. After physical examination blood and urine tests were provided. Results A 52-year-old male patient who had metastatic SCLC was admitted to the emergency unit because of fatigue, weakness and confusion. On physical examination the patient's face was darkened but his conjunctiva was pale, his tongue and mucous membranes were dry. The blood pressure was 90/60 mm Hg. The test results provided were as follows: Glucose 106 mg/dL, creatinine 0.42 mg/dL, urea 38.1 mg/dL, sodium 109 mmol/L, potassium 3.3 mmol/L, white blood cells 9760 /mm3, hemoglobin: 9 g/dL, platelets: 176000/mm3. The patient had no chemotherapy during the last three months. He also did not have a history of antihypertensive treatment. The echocardiographic examination revealed that the ejection fraction was 60%. The abdominal computerized tomography scan showed multiple metastasis of the tumor, but adrenal glands were free of metastasis. The sodium deficit was calculated targeting to 120 mmol/L and therapy was started. The patient's weight was 70 kg. The calculated sodium deficit was 420 mmol. Since the hyponatremia was chronic, the deficit was planned to be given in 24 hours. Potassium was also given. During hospitalization, on day 2nd the patient's blood and urine tests were as follows: Creatinine 0.58 mg/dL, urine creatinine 22.8 mg/dL, 24-hour urine volume 2200 mL, 24-hour creatinine clearance 60 ml/min. Urine sodium concentration 105.6 mmol/L, serum sodium 114 mmol/L, sodium clearance: 1.41 ml/min. Fractional sodium excretion was 2.3%. Although the treatment was continued for 6 days, with the same dose of 420 mEq sodium given for each day, the serum sodium concentration reached to 115 mmol/L on day 6. (Totally, 2520 mEq of sodium was given for 6 days). Therefore, hyponatremia was thought to be due to urinary loss of sodium. The fractional sodium excretion of 2.3% supported this. All these findings suggested the diagnosis of renal salt wasting in this patient. We decided to give the patient fludrocortisone (Astonin H 0.1 mg) twice a day orally in addition to sodium chloride tablets (approximately 1.5 gram = 25-30 mmol). During the follow-up of the patient, the both fludrocortisone pills and salt tablets increased to 2 × 2, finally, when reached the level of sodium is above 130 mmol/L, salt tablets were stopped. One thing need to be noted here; hyponatremia did not improve unless giving fludrocortisone. But after this, although more sodium was given during sodium replacement, there was no increase in fractionated sodium excretion, on the contrary, it decreased. On day 14th, Fractional sodium elimination was 1.7%. Serum Na: 133 mmol/L. The patient was advised to take fludrocortisone tablets twice a day orally and was discharged from hospital on day 15th when serum sodium concentration was 138 mmol/L. If a patient with serum cortisol level below 4 mcg/dl have been evaluated as adrenal insufficiency regardless of ACTH level in sera.; additionally, hyperpigmentation and hyponatremia due to salt wasting through the kidneys led us to diagnose. The hyponatremia resolved only after added fludrocortisone. Conclusion However SCLC can give rise euvolemic hyponatremia producing ADH generally, besides, SCLC can cause adrenal insufficiency leading to serious hypovolemic hyponatremia. Diagnose is of crucial importance for correct treatment which can be only achieved by replacing the both sodium and fludrocortisone.

#503 The influence of the degree of liver cell failure on the functional state of the kidneys in patients with liver cirrhosis

Abstract Background and Aims Studying the influence of the severity of liver cirrhosis on the functional ability of the kidneys in patients without concomitant diseases (without diabetes mellitus and hypertension). Method The study included 38 patients with liver cirrhosis who were treated in the gastroenterology department of the Republican Scientific and Practical Center for Therapy and Medical Rehabilitation in Tashkent. The average age of patients was 54 ± 3.4 (from 33 to 65). The examined patients were divided into two groups, depending on the degree of hepatic cellular failure (according to the Child-Pugh classification) and the development of ascitic syndrome. In group 1 Liver cirrhosis without ascites (P-P class A) the number of patients was 20. In group 2 Liver cirrhosis with ascites (P-P class B) the number of patients was 18. When examining patients, we used: Clinical blood test; blood chemistry; determination of electrolytes, creatinine; general urine analysis; glomerular filtration level; Functional renal reserve (defined as the increase in glomerular filtration expressed as a percentage after the administration of Dopamine at a dose of 2-3 μg/kg/min. To assess portal hypertension, all patients underwent ultrasound examination of the organs abdominal cavity and duplex scanning of portal system vessels. Results The examined patients were analyzed for the functional state of the kidneys and its relationship with the main parameters of portal hypertension and hepatic cell failure. Comparative characteristics of the main indicators of renal function significant differences in functional parameters were revealed depending on degree of hepatic cell failure. In the group of patients with cirrhosis with ascites, there was a significant decrease in renal GFR to 77.5 ± 1.4 ml/min, in contrast to the unchanged level of GFR in the group of patients with cirrhosis without ascites—99.3 ml/min. In patients with cirrhosis without ascites, the glomerular filtration rate increases by against the background of dopamine administration was 13.5 ± 4.7% (which corresponds to the norm), in contrast to patients in the second group, where the average Renal Functional Reserve was 8.4 ± 2.8%. Changes in renal function were also characterized by a decrease in Fractional Excretion of Sodium (FENa). The reduction in FENa in the group of patients with persistent ascites. During a detailed assessment of the RFR in patients of the first group, the RFR was below normal only in 2.6 ± 2.5%, while in the second group the number of patients with the decrease in the RFR was 69.7 ± 8.1%. Study of functional renal reserve in a group of patients with cirrhosis with ascites revealed unchanged this indicator in only 10 (30.3 ± 8%). U 19 (57.5 ± 8.6%) of patients in this group, the RFR was less than 10%, and in 12.2 ± 5.7% cases of RFR was below 5%, which indicated pronounced intraglomerular hypertension and the risk of developing resistant ascites. Conclusion The present study indicates that Renal Functional Reserve (RFR) in patients with liver cirrhosis reflects the speed of effective renal plasma flow. A decrease in FPR in Child-Pugh class A liver cirrhosis was detected in 2.6% of cases, with hepatic cell failure, Child-Pugh class B in 69.7%.

#2123 Ageing, renal function and frailty: analysis of the FRASNET study

Abstract Background and Aims Frailty is a common geriatric syndrome of significant public health importance. The kidney is one of the organs that progressively loses function with aging leading a decrease of glomerular filtration rate (GFR). In elderly the definition of eGFR threshold for the diagnosis of CKD is debated. FRASNET study aims of identify the role of kidney function (glomerular and tubular involvement) in determining frailty among not community-dwelling elderly adults, also depending on the genetics of each single subject. Method The FRASNET study was a cross-sectional multicentre observational cohort study involving healthy. The exclusion criteria were: i) severe cognitive impairment, ii) severe health problems. They have been characterised for BP, GFR, sodium intake (Kawasaki formula), cognitive status, quality of life, anamnestic factors, health and socio-economic status. Frailty was determined according to modified Fried index by the presence of three conditions among reduced grip strength, reduced gait speed, low physical activity, self-reported exhaustion. We considered the number of drugs as an index of comorbidity. Genotyping of 20 targeted single nucleotide polymorphisms (SNPs) selected on renal and hypertension was performed. ANOVA and conditional inference tree analysis have been carried out. Results 1183 individuals were included in the study sample. Median age was 72 [IQ 69-77]. 328 (27.7%) subjects were robust, 445 (37.6%) pre-frail, 410 (34.7%) frail. Frailty increases with age, especially after 75 years (from 28.9% to 75.7%). The overall mean GFR was 71.8 ± 16.5 ml/min/1.73 m2. Estimated 24 h urinary sodium excretion was 194.5 mEq/24 h with median fractional excretion of sodium (FeNa) 0.75%. In 31.9% of sample FeNa was greater than 1%. Only 3% of subjects reported CKD. Moreover, 21.1% presented eGFR ≤ 60 and the prevalence of CKD increases according to age from 12.3% to 70.3%. CKD prevalence increases in linear manner across frailty classes from 20% in robust to 47.6% in frail. Conditional inference tree analysis confirmed the role of age, comorbidity and GFR in determining frailty. In oldest subjects (>75 years old), the eGFR level most strongly associated with frailty was below 53 (ml/min/1.73 m2) (Fig. 1). No differences in sodium excretion were observed according to frailty classes. Moreover, we observed an increase of FeNa according to age and frailty classes form 0.71% (median (IQR 0.567)) to 0.79% (median (IQR 0.690)). In frail group exaggerated FeNa (>1%) is more frequent than in robust and pre-frail subjects (Chi-squared p = 0.021). Even after the introduction of these variables in inferential trees the new proposed cut-off for GFR (53) is a main determinant of frailty in oldest (Fig. 2). The eGFR parameter resulted associated with two genetic variants in RAAS system, rs5051 in the angiotensinogen gene (AGT) and rs2131127 in the angiotensin II receptor type 1 (AGTR1). The rs4293393 in uromodulin gene (UMOD) was confirmed associated with eGFR value. Conclusion The present study is part of the complex debate on the relationship among renal function, aging and frailty. We can therefore conclude that glomerular filtration (eGFR below 50 and not the presence of CKD) must be considered among the factors that influence frailty. Our study also showed a deterioration of tubular function in frail subject that can be expression of structural changes due to nephroangiosclerosis.

A Comparative Analysis of Fractional Excretion of Sodium, Potassium and Magnesium among T2DM Patients with Increased Albuminuria and Normal Albuminuria in a Tertiary Care Hospital- An Observational Study

Background: T2DM often leads to diabetic kidney disease, a condition marked by change in GFR and urinary albumin excretion. The renal handling of key electrolytes like sodium, potassium, and magnesium plays a crucial role in the progression of renal tubulointerstitial damage in diabetic patients. Aim of the study: The aim of this study was to compare the fractional excretion of sodium, potassium and magnesium among T2DM patients with increased albuminuria and normal albuminuria. Methods: This observational study was conducted in Department of Nephrology, Chattogram, Bangladesh from February 2021 to January 2022. Total 125 patients with T2DM were included in this study. Result: Baseline characteristics showed no significant differences across the study groups. Biochemically, eGFR decreased non-significantly from 95.5 to 86.1 ml/min/1.73 m² across groups, while UACR significantly increased from 14.3 to 1056 mg/gm (P<0.001). FBG levels were similar, but 2hPPBG showed a significant decrease from 8.2 to 7.4 mmol/l (P=0.0041). HbA1C levels varied slightly. FENa, FEK, and FEMg showed significant differences across groups, with FENa ranging from 0.59% to 0.56% (P=0.0016), FEK from 9.4% to 6.9% (P=0.0358), and FEMg from 2.87% to 5.58% (P=0.001). Correlations revealed significant negative associations of eGFR with FENa, FEK, and FEMg, and a significant positive correlation of FEMg with UACR. No significant correlations were found between FBG, 2hPPBG, HbA1C, and the electrolytes excretion. Conclusion: Significant variations in the fractional excretion of sodium, potassium, and magnesium were observed. Higher eGFR was associated with lower electrolyte excretion, and a significant positive correlation was found between magnesium excretion and UACR.

Short-term effects of small volume saline infusion on acid base equilibrium in critically ill patients.

Short-term acid-base effects of 0.9% saline solution infusion are not well described. Aim of this study was to assess the effects of a fluid challenge with 0.9% saline in critically ill patients according to the Stewart's approach, which allows a precise determination of acid base equilibrium. In 40 mechanically ventilated critically ill patients, acid-base variables according to Stewart's approach were measured before and after 30 minutes from the infusion of 0.5L of 0.9% saline. Patients were divided in saline responder (fractional sodium excretion increase <0.5) and non-responders, and in patients with (estimated glomerular filtration rate >63 mL/min) and without renal impairment. After saline infusion, plasma sodium concentration did not change (138 [135-141] vs. 138 [135-140] mEq/L, P=0.646), while chloride concentration significantly increased (102 [100-106] vs. 104 [191-106] mEq/L, P=0.003), reducing strong ion difference (37.0 [34.9-38.0] vs. 35.4 [32.7-37.5] mEq/L, P=0.004) without any impact on pH, due to the concomitant albumin dilution. In saline non-responders, the increase of plasma chloride concentration caused a reduction in strong ion difference, while in saline responders both plasma chloride concentration and strong ion difference remained similar. Patients with and without renal impairment presented a similar acid-base response. The infusion of 0.9% saline reduced strong ion difference by increasing plasma chloride concentration, with no effect on pH due to concomitant albumin dilution. Saline non-responders, characterized by the ability to excrete the sodium excess, were more likely to suffer the acidifying effects of saline infusion, while renal function did not affect the acid-base response to saline infusion.

The association between hemoglobin levels and renal function parameters during normothermic machine perfusion: A retrospective cohort study using porcine kidneys.

Ex vivo normothermic machine perfusion (NMP) is a promising tool for assessing an isolated kidney prior to transplantation. However, there is no consensus on the perfusate's optimal oxygen-carrying capacity to support renal function. To investigate the association of hemoglobin levels with renal function parameters, a retrospective analysis of isolated, normothermically, perfused porcine kidneys was performed. Between 2015 and 2021, a total of 228 kidneys underwent 4 h of NMP with perfusates that varied in hemoglobin levels. A generalized linear model was used to determine the association of hemoglobin levels with time-weighted means of renal function markers, such as fractional sodium excretion (FENa) and creatinine clearance (CrCl). Stratified by baseline hemoglobin level (<4.5, 4.5-6, or >6 mmol/L), these markers were modeled over time using a generalized linear mixed-effects model. All models were adjusted for potential confounders. Until a hemoglobin level of around 5 mmol/L was reached, increasing hemoglobin levels were associated with superior FENa and CrCl. Thereafter, this association plateaued. When hemoglobin levels were categorized, hemoglobin <4.5 mmol/L was associated with worse renal function. Hemoglobin levels were neither significantly associated with proteinuria during NMP nor with ATP levels at the end of NMP. Hemoglobin levels >6 mmol/L showed no additional benefits in renal function. In conclusion, we found an association between baseline hemoglobin levels and superior renal function parameters, but not injury, during NMP of porcine kidneys. Furthermore, we show that performing a retrospective cohort study of preclinical data is feasible and able to answer additional questions, reducing the potential use of laboratory animals.

Prolonged renal function impairment in infants born during the peri-viable period: A retrospective longitudinal cohort study

BackgroundThe number of infants born during the peri-viable period who survive has been increasing. AimTo clarify renal function in infants from the time of birth during the peri-viable period until their due date. Study designThis retrospective cohort study was conducted at a single center. SubjectsWe reviewed the data of infants born at ≤28 weeks of gestation between 2018 and 2022 at our hospital. The infants were divided into the following groups: born at 22–24 weeks vs. 25–28 weeks (appropriate-for-gestational age [AGA] infants), and AGA infants vs. small-for-gestational age (SGA) infants (born at 22–28 weeks). Outcome measuresWe compared the perinatal data and renal function of the infants from birth until their due date. ResultsEighty-one infants were included. Their serum creatinine, fractional excretion of sodium, and urine glucose levels were high or positive soon after birth but gradually improved. The urine albumin level was significantly higher among AGA infants born at 22–24 weeks, even at term equivalent age, than among those born at 25–28 weeks. ConclusionsPersistent renal insufficiency was observed even around the term equivalent age in peri-viable infants. Follow-up data collected after the neonatal period should be investigated in these infants.

Hepatorenal Syndrome Type 1: Diagnosis and Treatment

Hepatorenal Syndrome Type 1: Diagnosis and Treatment

767 - Fractional excretion of urinary sodium and urinary sediment microscopy for prediction of response to vasoconstrictors in hepatorenal syndrome type 1

767 - Fractional excretion of urinary sodium and urinary sediment microscopy for prediction of response to vasoconstrictors in hepatorenal syndrome type 1

Does Hypertension Affect the Recovery of Renal Functions after Reversal of Unilateral Ureteric Obstruction?

Research has demonstrated that hypertension can lead to an exaggeration in the renal functional and histological changes caused by ureteral obstruction. These changes were particularly observed shortly after the release of a relatively brief period of unilateral ureteral obstruction (UUO). However, the long-term impact of hypertension on the recovery of renal functions has not been investigated beyond the immediate period after UUO reversal. In order to investigate this effect, a group of spontaneously hypertensive rats (G-SHR, n = 11) and a group of normotensive Wistar Kyoto rats (G-NTR, n = 11) were subjected to a 48 h reversible left UUO. The impact of UUO was then examined 45 days after the reversal of obstruction. The glomerular filtration rate, renal blood flow, and the fractional excretion of sodium in the post-obstructed left kidney (POK) showed similarities to the non-obstructed right kidney (NOK) in both groups. However, the changes in the albumin creatinine ratio, renal injury markers, pro-apoptotic markers, and histological changes in the G-SHR were much more pronounced compared to the G-NTR. We conclude that hypertension continues to have a significant impact on various aspects of renal injury and function, even several weeks after UUO reversal.

Clinicopathologic Study of Sickle Cell-associated Kidney Disease: A Nigerian Experience.

Improvements in sickle cell disease (SCD) care have resulted in the survival of many patients into adulthood, although this is accompanied by the increased incidence of end-organ damage, including chronic kidney disease (CKD). This study assessed the prevalence, pattern and predictors of renal dysfunction in SCD patients and investigated the associated renal histopathologic changes. We evaluated 105 patients with SCD, for proteinuria, estimated glomerular filtration rate (eGFR), and tubular dysfunction. Renal biopsy was conducted on 22 patients who qualified. Data were analysed using SPSS package version 23. Thirty-seven (35.2%) of the 105 patients had CKD, as defined by an eGFR of 60 ml/min/1.73 m2 and/or proteinuria. The fractional excretion of potassium (FEK) was elevated in all patients, whereas the fractional excretion of sodium (FENa) was elevated in 98.1%. Glomerular filtration rate was negatively correlated with irreversible percentage sickle cell count (r = -0.616, P = 0.0001), FEK (r = -0.448, P = 0.0001) and FENa (r = -0.336, P = 0.004). Age, irreversible percentage sickle cell count, haemoglobin levels and FENa were the major predictors of CKD. The histological pattern in the 22 patients who had biopsies was consistent with mesangioproliferative glomerulonephritis 11 (50%), minimal change disease 6 (27.3%), focal segmental glomerulosclerosis 3 (13.6%) and interstitial nephritis 2 (9.1%). CKD was prevalent in SCD patients, and it was characterised by tubular dysfunction and mesangioproliferative glomerulonephritis. The main predictors of CKD were increased age, severity of vaso-occlusive crisis, worsening anaemia and tubular dysfunction.

Furosemide attenuates tubulointerstitial injury and allows functional testing of porcine kidneys during normothermic machine perfusion.

Normothermic machine perfusion (NMP) is a promising pretransplant kidney quality assessment platform, but it remains crucial to increase its diagnostic potential while ensuring minimal additional injury to the already damaged kidney. Interventions that alter tubular transport can influence renal function and injury during perfusion. This study aimed to determine whether furosemide and desmopressin affect renal function and injury during NMP. Eighteen porcine kidneys (n = 6 per group) were subjected to 30 min of warm ischemia and 4 h of oxygenated hypothermic perfusion before being subjected to 6 h of NMP. Each organ was randomized to receive no drug, furosemide (750 mg), or desmopressin (16 μg) during NMP. Compared with the other groups, the addition of furosemide resulted in significantly increased urine output, fractional excretion of sodium and potassium, and urea clearance during NMP. Urinary neutrophil gelatinase-associated lipocalin levels decreased significantly with furosemide supplementation compared with the other groups. The addition of desmopressin did not result in any significantly different outcome measurements compared with the control group. This study showed that the addition of furosemide affected renal function while attenuating tubulointerstitial injury during NMP. Therefore, furosemide supplementation may provide renal protection and serve as a functional test for pretransplant kidney viability assessment during NMP.

Impact of vasodilators on diuretic response in patients with congestive heart failure: A mechanistic trial of cimlanod (BMS-986231).

To investigate the effects of Cimlanod, a nitroxyl donor with vasodilator properties, on water and salt excretion after an administration of an intravenos bolus of furosemide. In this randomized, double-blind, mechanistic, crossover trial, 21 patients with left ventricular ejection fraction <45%, increased plasma concentrations of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and receiving loop diuretics were given, on separate study days, either an 8 h intravenous (IV) infusion of cimlanod (12 μg/kg/min) or placebo. Furosemide was given as a 40 mg IV bolus four hours after the start of infusion. The primary endpoint was urine volume in the 4 h after the bolus of furosemide during infusion of cimlanod compared with placebo. Median NT-proBNP at baseline was 1487 (interquartile range: 847-2665) ng/L. Infusion of cimlanod increased cardiac output and reduced blood pressure without affecting cardiac power index consistent with its vasodilator effects. Urine volume in the 4 h post-furosemide was lower with cimlanod (1032 ± 393 ml) versus placebo (1481 ± 560 ml) (p = 0.002), as were total sodium excretion (p = 0.004), fractional sodium excretion (p = 0.016), systolic blood pressure (p < 0.001), estimated glomerular filtration rate (p = 0.012), and haemoglobin (p = 0.010), an index of plasma volume expansion. For patients with heart failure and congestion, vasodilatation with agents such as cimlanod reduces the response to diuretic agents, which may offset any benefit from acute reductions in cardiac preload and afterload.

Serum and Urinary Matrix Metalloproteinase-9 Concentrations in Dehydrated Horses.

Matrix metalloproteinase-9 is increased in renal tissue in human kidney disease, but its role as a biomarker for kidney disease has not been fully evaluated yet. The aim of this study was to evaluate serum MMP-9 (sMMP-9) and urinary MMP-9 (uMMP-9) concentrations in dehydrated horses. Dehydrated horses were prospectively included. Blood and urinary samples were taken at admission, and after 12, 24, and 48 h (t0, t12, t24, t48), an anti-equine MMP-9 sandwich ELISA was used. Four healthy horses served as the controls. Serum creatinine, urea, symmetric dimethylarginine (SDMA), urine-specific gravity, urinary protein concentration, fractional sodium excretion, and urinary gamma-glutamyl transferase/creatinine ratio (uGGT/Cr) were measured. Statistical analysis included a repeated measures ANOVA and mixed linear regression model. Overall, 40 dehydrated horses were included (mild dehydration 13/40, moderate 16/40, severe 11/40). Acute kidney injury was found in 1/40 horses; 7/40 horses showed elevated serum creatinine, 11/40 horses elevated serum SDMA, and 5/28 elevated uGGT/Cr at presentation. In dehydrated horses, sMMP-9 concentrations were significantly higher on t0 (median: 589 ng/mL, range: 172-3597 ng/mL) compared to t12 (340 ng/mL, 132-1213 ng/mL), t24 (308 ng/mL, 162-1048 ng/mL), and t48 (258 ng/mL, 130-744 ng/mL). In healthy horses, sMMP-9 (239 ng/mL, 142-508 ng/mL) showed no differences over time or compared to patients. uMMP-9 and uMMP-9/creatinine did not differ over time or to the controls. No differences were found between dehydration groups. Urinary casts (p = 0.001; estimate = 135) and uGGT/Cr (p = 0.03; estimate = 6.5) correlated with sMMP-9. Serum urea was associated with uMMP-9/Cr (p = 0.01, estimate 0.9). In conclusion, sMMP-9 was elevated at arrival in dehydrated patients compared to later measurements. Correlations to uGGT/Cr and urinary casts need further evaluation.

Fractional Excretion of Urinary Sodium and Urinary Sediment Microscopy for Prediction of Response to Vasoconstrictors in Hepatorenal Syndrome Type 1

Fractional Excretion of Urinary Sodium and Urinary Sediment Microscopy for Prediction of Response to Vasoconstrictors in Hepatorenal Syndrome Type 1

Fractional Excretion of Urea for the Differential Diagnosis of AKI: A Systematic Review and Meta-Analysis with Comparison to Fractional Excretion of Sodium

Fractional Excretion of Urea for the Differential Diagnosis of AKI: A Systematic Review and Meta-Analysis with Comparison to Fractional Excretion of Sodium

Contribution of thick ascending limb and distal convoluted tubule to glucose-induced hypercalciuria in healthy controls.

Carbohydrates increase kidney stone risk and increase urine calcium and magnesium. We hypothesize that the effects of glucose as an allosteric modulator of calcium-sensing receptors may mediate this effect. Six healthy subjects were on a low-sodium diet before consuming 100 g of glucose beverage. Timed fasting (3) and postglucose (6) urine and blood samples were collected every 30 min. Urine composition and serum markers were measured and microvesicular abundance of tubular transport proteins (NHE3, NKCC2, NCC, and TRPV5) were quantified. Postglucose, serum glucose, and insulin rose rapidly with a parallel increase in calcium and magnesium excretion and no change in fractional excretion of sodium. Both serum parathyroid hormone (PTH) and urine TRPV5 fell in the postglucose periods. The rise in the calcium and magnesium excretion likely occurred primarily in the thick ascending limb where they are both under control of the calcium-sensing receptor. The fall in PTH and TRPV5 support the role of glucose as an allosteric modulator of calcium-sensing receptor.NEW & NOTEWORTHY Sugar increases urine calcium and magnesium as well as kidney stone and bone disease risk. Our study provided new insights into the underlying mechanism as we gave healthy subjects an oral glucose load and used newer tools such as fractional excretion of lithium, serum parathyroid hormone, and microvesicular abundance of tubular transport proteins to characterize the mechanism and identify the thick ascending limb with possible calcium-sensing receptor mediation as a likely contributor to this mechanism.

THU280 Acute Interstitial Nephritis- A Complication Of Semaglutide Use

Abstract Disclosure: M. Alsayed Hasan: None. J. Doroshow: None. Background: With the widespread use of glucagon-like peptide 1 (GLP-1) agonists in diabetes, several cases have been reported of GLP-1 induced acute interstitial nephritis (AIN) with variable recovery in kidney function (1). Although it is a rare side effect, the primary management requires early identification and removal of the offending agent. Clinical Case: A 75-year-old male presented with a week of nausea, vomiting, abdominal pain, and reduced urine output. He was started on semaglutide 4 months prior to admission when his creatinine was 1.16 mg/dL. Initial lab abnormalities included an elevated blood urea nitrogen 119 mg/dL (n 8-20 mg/dL), elevated creatinine 13.8 mg/dL (n 0.7-1.3 mg/dL), anion gap acidosis with a CO2 of 15 mEq/L (n 22-32 mEq/L) and an anion gap of 18 (n&amp;lt;12), lipase 659 U/L (n 20-51 U/L). His urinalysis demonstrated too numerous to count red blood cells, 4-10 white blood cells, rare eosinophils and no casts or crystals. Urine culture was negative. The fractional excretion of sodium and urea were 5.56% and 56% respectively, consistent with intrinsic renal disease. CT of the abdomen and pelvis demonstrated peri-pancreatic inflammation. A follow up renal ultrasound showed normal echotexture with no hydronephrosis or renal calculi. His picture was concerning for pancreatitis and pre-renal/acute tubular necrosis from diuretic use and vomiting. Despite aggressive fluid resuscitation, there was minimal improvement in his creatinine. Further work up for his renal injury was negative for monoclonal antibodies on protein electrophoresis and immunofixation. An autoimmune work up was negative for antinuclear antibody, anti-double stranded DNA, antineutrophil cytoplasmic (ANCA) myeloperoxidase IgG, anti-proteinase 3 ANCA IgG, glomerular basement membrane antibody, hepatitis B and C antibodies, and HIV. Complements and immunoglobin G subclasses were normal. A renal biopsy was performed which showed active interstitial inflammation with eosinophils consistent with allergic interstitial nephritis without an immune complex mediated glomerular lesion. He was started on intravenous methyl prednisone for 3 days followed by a prednisone taper. His home metformin, ramipril and hydrochlorothiazide were discontinued on discharge. He was eventually started on mycophenolate as the creatinine did not return to baseline with steroids. Conclusion: AIN is a rare, yet serious complication of GLP-1 use that requires early identification and discontinuation of the medication. A rapid or unexplained decline in renal function after starting a GLP-1 should be evaluated early on with concern for AIN once volume depletion is ruled out (1). Reference: (1) Chaudhury N., Liarakos A., Gopalakrishnan K., Ayub W., Murthy N., Rao R. Antidiabetic medication-induced acute interstitial nephritis: case report and literature search. British Journal of Diabetes. 2021;21(2);228-32. Presentation: Thursday, June 15, 2023

Role of urinary fractional excretion of sodium in resistant hypertension patients

Role of urinary fractional excretion of sodium in resistant hypertension patients

Serial evaluation of loop diuretic efficiency following left ventricular assist device implantation.

More than 50% of heart failure (HF) patients require diuretic therapy after left ventricular assist device (LVAD). Although few data related to diuretic response (DR) exist in stage D patients, tubular sodium reabsorption may be clinically prognostic independent of estimated glomerular filtration rate (eGFR) and proteinuria within this cohort. We aimed to characterize DR serially before and after LVAD implantation in a stage D population. We conducted a prospective, observational cohort study of HF patients receiving diuretics with plans to undergo LVAD implantation. We measured urine sodium (UNa) and creatinine (UCr) at three points after diuretic therapy: pre-LVAD, post-LVAD prior to discharge, and as an outpatient. Prior to LVAD, patients (N = 19) had an average eGFR of 54.0 ± 18.0 mL/min/1.73 m2, spot UNa of 74.8 ± 28.0 mmol/L, and fractional excretion of sodium (FENa) of 3.1 ± 2.7%. Pre-LVAD, eGFR did not correlate with spot UNa nor FENa (p > 0.05 for both). LVAD implantation did not improve DR post-LVAD (mean change FENa per 40 mg IV furosemide 0.5 ± 1.0%; p = 0.84), and 90% of patients required loop diuretics at 90 days post-surgery. Improved hemodynamics following LVAD may not improve DR or tubular function; larger studies are needed to confirm our results and assess the utility of DR to predict post-LVAD outcomes.