24-hour Urine Collection Research Articles

Association Between Dietary Potassium Intake Estimated From Multiple 24-Hour Urine Collections and Serum Potassium in Patients With CKD

Limited and inconclusive evidence for the association of dietary potassium intake with serum potassium in chronic kidney disease (CKD) patients have been shown, though restricting dietary potassium has been recommended for CKD patients to prevent hyperkalemia. Multiple 24-hour urine collections are necessary to adequately assess potassium intake. We investigated associations of 24-hour urinary potassium excretion (UKV) with serum potassium in CKD outpatients based on multiple 24-hour urine collections. This retrospective cohort study was based on outpatients with CKD stages G3 to G5, median age of 72.0 years; and median follow-up of 3.9 months and 8.9 months, respectively, for analyses using 3-time measurement (N= 290 and 870 observations) and 7-time measurements (N= 220 and 1540 observations). The outcome was serum potassium. Multivariable-adjusted mean difference in serum potassium (mEq/l) and odds ratio of hyperkalemia per 10 mEq/d increase in UKV were, respectively, 0.12 (95% confidence interval [CI]: 0.09-0.15) and 2.15 (1.70-2.73) in generalized estimating equations (GEEs) with 3-time measurements. The mean difference became more pronounced as CKD stages progressed: 0.08 (0.05-0.12), 0.12 (0.08-0.16), and 0.16 (0.12-0.20) for CKD G3, G4, and G5. Similar results were obtained from analyses using 7-time measurements and hierarchical Bayesian measurement error models treating measurement error of UKV adequately. We suggest significant but weak associations (R2: 0.08, 0.14, and 0.18 for CKD G3, G4, and G5) between serum potassium and dietary potassium intake estimated by multiple 24-hour urine collections in CKD patients. Further studies are needed to validate nutritional and clinical aspects of the associations.

The Severity of Obesity Promotes Greater Dehydration in Children: Preliminary Results.

The state of hydration of the body depends on the balance between the amount of water and salt consumed and excreted (the urinary extraction of excess sodium requires water). Inappropriate nutrition, particularly consuming too much processed food, causes obesity in children and additionally causes excessive sodium consumption, thus increasing the risk of excessive water loss. The aim of this study was to assess the hydration status of children with obesity and the relation between hydration, body composition, urinary sodium extraction, and nutrient intake. The study group consisted of 27 patients with obesity, with a mean age of 12.89 ± SD 2.79. Each patient's height, weight, body composition (electrical bioimpedance (BIA)), diet (7-day record), and biochemical tests were assessed. The hydration status was assessed using 24-hour urine collection, 24-hour urine osmolality, and an ultrasound of the vena cava (IVC/Ao index). Overall, 55% of children (n = 15) had urine osmolality values above 800 mOsm/kgH2O, which indicates significant dehydration, and 53% (n = 14) were dehydrated, based on the IVC/Ao index. Children with obesity and dehydration had a significantly higher BMI (31.79 vs. 27.32; p = 0.0228), fat mass percentage (37.23% vs. 30.07% p = 0.0051), and fat mass in kg (30.89 vs. 20.55; p = 0.0158), and significantly higher sodium intake from their diet (3390.0 mg vs. 2921.0 mg; p = 0.0230), as well as their sodium/potassium ratio (2.4 vs. 2.0; p = 0.0043). The 24-hour urinary sodium excretion and osmolality values were directly related to fat-mass percentage and fat-mass (in kg) in a simple linear correlation analysis. Our preliminary results confirm that obesity is related to dehydration. The overall high sodium excretion in children with obesity indicates an excessive salt intake along with low potassium intake, which is a significant predictor of dehydration, regardless of the total water intake (TWI).

Urinary Melatonin Metabolite in Premature Infants with Extremely and Very Low Birth Weight

The aim. Determination of daily urinary 6-sulfatoxymelatonin in premature infants with extremely and very low birth weight. Materials and methods. A non-invasive, descriptive, single-centered study involving data of 96 premature infants with weight less than 1500 g : 46 infants with extremely and 50 infants with very low birth weight. The study included a detailed scrutiny of history and objective examinations, data from medical records, anthropometric measurements, and daily urine collection. Determination of 6 - SM in the 24-hours urine collection from premature infants was performed by enzyme immunoassay on the analyzer “Labline-90” (Austria) using a commercial test system manufactured by “LDR” (LABOR DIAGNOSTIKA NORD GmbH & Co.KG, Germany) according to the provided instruction. 166 portions of urine were collected during the examination in time intervals: 96 portions of urine in premature infants at 1st day of life and 70 portions at 10th – 14th day of life. Results. Ante- and intranatal periods for the infants enrolled in the study were characterized by conditions: premature rupture of membranes 37 (38.5%), multiple pregnancy 16 (16.6%), preeclampsia 15 (15.6%), isthmic-cervical insufficiency 11 (11.5%), placental abruption 8 (8.3%), extra corporal fertilization 5 (5.2%), chorioamnionitis 4 (4.2%); caesarean section urgent 33 (34.4%) and planned 24 (25.0%). There was no any significant difference in frequency of ante – and intranatal pathology between ELBW and VLBW. Antenatal administration of corticosteroids for reduce the severity of neonatal respiratory distress syndrome occurred in all mothers of infants enrolled in the study. There was significant low urinary 6-sulfatoxymelatonin level in extremely low birth weight infants (median 120.0 pg /mL) on the 1st day of life compared with very low birth weight (median 348.5 pg / mL). There was no difference at 10 – 14th days. The predictive level of lethal outcome in infants with extremely low birth weight is ≤ 84 pg / mL with sensitivity 84.62% and specificity 70.0%. Conclusion. In infants with extremely and very low birth weight the determining the urinary 6-sulfatoxymelatonin is a non-invasive method. The significant decrease level of urinary 6-sulfatoxymelatonin in infants with extremely low birth weight on the first day of life was found. The measurement of urinary 6-sulfatoxymelatonin will allow to establish the prediction of perinatal outcomes. Its levels <87 pg / mL is associated with lethal outcomes. Authors speculate than it will the way for future supplement of melatonin to premature infants and study of its effect on perinatal outcomes

Abstract 11319: Post-Operative Dialysis in Failing Fontan Patients Undergoing Heart Transplant: How Well Does the Pre-Transplant Creatinine Clearance Risk-Stratify Patients?

Introduction: The need for dialysis early post-heart transplant (HT) can be suprisng when it occurs in the setting of purportedly normal renal function pre-HT, as has been described in failing Fontan (FF) patients. Hypothesis: We hypothesized that FF patients may have an increased incidence of post-operative dialysis (POD). Methods: The Pediatric Heart Transplant Society (PHTS) database was used to identify all children ≥2 years of age with failing Fontan (FF) physiology or cardiomyopathy (CM, benchmark lesion) who underwent isolated HT from 2005-2019. The primary endpoint was POD, defined as any form of dialysis within the first 30 days post-HT. Pre-transplant estimated glomerular filtration rate (eGFR) was calculated using the modified Schwartz formula, and a subset of patients with provided supplemental data additionally had renal function evaluated by a non-creatinine-based method. Results: Of 2003 children who met the inclusion criteria, 263 had FF (13%) and 1740 had CM (87%). Whereas the mean ages were similar (FF 11.2 vs CM 12.2 years, P=0.3), FF patients were 11% shorter (134 vs. 148, P<0.001) and 9 kg lighter (31.2 vs. 40.2, P<0.001), and had a lower serum creatinine (0.57 vs. 0.64 mg/dl, P=0.001) but similar eGFR pre-transplant (110.2 vs. 106.7 L/min/1.73m 2 , P=0.26). In a subset of 22 FF patients with available results from 24-hour urine collection or nuclear medicine scan, the Schwartz formula overestimated the GFR in 15/22 patients by an average of 40.2 ml/min/1.73 m2 (range 2.6 to 91.8). Overall, compared to CM patients, FF patients had a 4.7-fold higher risk of requiring POD (3.8% vs. 0.8%, P<0.001). Of those who required POD, the difference in 30 day post-HT mortality was not significant (40% vs. 14%, 0.3). Multivariable analysis revealed that pre-HT ECMO and longer CPB times were independently associated with POD; there was a trend toward association of higher pre-HT eGFR (P=0.06). Conclusions: Fontan patients have a ~5-fold higher risk of post-operative dialysis compared to cardiomyopathy patients, and despite a normal or even supraphysiological pre-transplant estimated CrCl. Non-creatinine-based methods independent of malnutrition status should be considered in the FF population.

Association of the Urine-to-Plasma Urea Ratio With CKD Progression

The urine-to-plasma (U/P) ratio of urea is correlated with urine-concentrating capacity and associated with progression of autosomal dominant polycystic kidney disease. As a proposed biomarker of tubular function, we hypothesized that the U/P urea ratio would also be associated with progression of more common forms of chronic kidney disease (CKD). Observational cohort study. 3,723 adults in the United States with estimated glomerular filtration rate (eGFR) of 20-70 mL/min/1.73 m2, enrolled in the Chronic Renal Insufficiency Cohort (CRIC) Study. U/P urea ratio, calculated from 24-hour urine collections and plasma samples at baseline. Associations of U/P urea ratio with eGFR slope, initiation of kidney replacement therapy (KRT), and CKD progression, defined as 50% decline in eGFR or incident KRT. Multivariable linear mixed-effects models tested associations with eGFR slope. Cox proportional hazards models tested associations with dichotomous CKD outcomes. The median U/P urea ratio was 14.8 (IQR, 9.5-22.2). Compared with participants in the highest U/P urea ratio quintile, those in the lowest quintile had a greater eGFR decline by 1.06 mL/min/1.73 m2 per year (P< 0.001) over 7.0 (IQR, 3.0-11.0) years of follow-up observation. Each 1-SD lower natural log-transformed U/P urea ratio was independently associated with CKD progression (HR, 1.22 [95% CI, 1.12-1.33]) and incident KRT (HR, 1.22 [95% CI, 1.10-1.33]). Associations differed by baseline eGFR (P interaction= 0.009). Among those with an eGFR≥30 mL/min/1.73 m2, each 1-SD lower in ln(U/P urea ratio) was independently associated with CKD progression (HR, 1.30 [95% CI, 1.18-1.45]), but this was not significant among those with eGFR<30 mL/min/1.73 m2 (HR, 1.00 [95% CI, 0.84-1.20]). Possibility of residual confounding. Single baseline 24-hour urine collection for U/P urea ratio. In a large and diverse cohort of patients with common forms of CKD, U/P urea was independently associated with disease progression and incident kidney failure. Associations were not significant among those with advanced CKD at baseline.

Attenuated Relationships Between Indexes of Volume Overload and Atrial Natriuretic Peptide in Uncontrolled, Sustained Volume-Dependent Primary Hypertension.

Whether systolic blood pressure (SBP) control in sustained volume-dependent primary hypertension is associated with blunted ANP (atrial natriuretic peptide) relationships with indexes of volume load is unknown. Systemic hemodynamics (central pressure, echocardiographic aortic velocity and diameter measurements in the outflow tract), circulating ANP concentrations (ELISA assays) and glomerular and tubular function (24-hour urine collections [n=519]) were determined in a community of African ancestry (n=772). As compared with those with a controlled SBP, those with an uncontrolled SBP (n=198) showed lower ANP concentrations (P<0.005) despite higher stroke volume and cardiac output (P<0.0001) and renal differences consistent with enhanced fluid retention. In those with a controlled SBP, fractional Na+ excretion (FeNa+; P<0.0005) and creatinine clearance (glomerular filtration rate; P<0.005) were inversely associated with ANP concentrations independent of confounders. Moreover, in those with a controlled SBP, stroke volume and cardiac output (P<0.0001) were independently and positively associated with ANP concentrations. In addition, in those with a controlled SBP, ANP concentrations were independently and inversely associated with systemic vascular resistance (SVR; P<0.0001) and aortic characteristic impedance (Zc; P<0.005). By contrast, in those with uncontrolled SBP, no relationships between either stroke volume (P>0.25), cardiac output (P>0.29), FeNa+ (P>0.77), or glomerular filtration rate (P>0.47) and ANP concentrations were noted. Furthermore, in those with an uncontrolled SBP, no relationships between ANP concentrations and SVR or Zc were observed (P>0.34). In a population where primary hypertension is strongly volume-dependent, those with an uncontrolled SBP have an attenuated relationship between ANP and both renal and hemodynamic indexes of volume overload and the vascular effects of ANP.

PMON88 A Rare Case of Composite Paraganglioma in the Bladder

Abstract Background Paragangliomas are neuroendocrine tumors that arise from embryonic neural crest cells; they are essentially extra-adrenal pheochromocytomas most frequently found in the head and neck. Composite tumors are rare and consist of the presence of two histologically distinct tissues within a single tumor. Additionally rare is the presence of a composite paraganglioma in the retroperitoneum and urinary bladder, of which there are few reported cases. Case Report We present a case of a 57 year old female who was found to have an incidental pelvic mass noted to progressively increase in size over the years on subsequent imaging. The patient had a cystoscopy and retrograde pyelogram that were both unremarkable. MRI Pelvis showed a 1.8×1.8×1.9 cm rounded, well-circumscribed lesion at the left posterior lateral bladder extending exophytically from the serosa at the ureterovesicular junction. As she had associated hypertension, palpitations, and anxiety, the patient was evaluated for pheochromocytoma.Laboratory workup showed elevated plasma levels of free Metanephrines at 130 (&amp;lt;57 pg/mL), free Normetanephrines at 247 (&amp;lt;148 pg/mL), and a free Total level at 377 (&amp;lt;205 pg/mL). 24-hour urine collection was consistent with mild elevation of Metanephrines at 330 (90-315 mcg/24 h), normal levels of Normetanephrines at 469 (122-676 mcg/24 h), and normal levels of Total urine Metanephrines of 799 (224-832 mcg/24 h). 24-hour urine free Catecholamines showed: Epinephrine of 6 (2-24 mcg/24 h), Norepinephrine of 77 (15-100 mcg/24 h), and a Total (Epi+NE) of 83 (26-121 mcg/24 h), with Dopamine of 220 (52-480 mcg/24 h).Due to mildly elevated metanephrine levels, the patient was started on the alpha-blocker doxazosin. She ultimately underwent a laparoscopic removal of the bladder mass, with pathology reports confirming presence of a composite paraganglioma with atypical features. Additionally, further immunohistochemistry was negative for the SDHB gene mutation in the tissue samples obtained. Conclusion Composite paragangliomas of the urinary bladder are very rare. Certain genetic pathologic variants carry an increased risk for malignancy and possible metastasis; therefore, these neuroendocrine tumors usually require targeted mutation testing. At this time, the pathogenesis of composite paragangliomas is still largely unknown, with little information available about treatment options and clinical outcomes. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

PSUN61 Primary Aldosteronism Presenting as Chronic Hypokalemia in a Normotensive Patient

Abstract Introduction Conn first described the hallmark features of primary aldosteronism (PA) as a state of aldosterone excess in the setting of hypertension and hypokalemia. Recent work has shed light on a wide spectrum of disease that likely includes normotensive patients with elevated aldosterone and suppressed renin. Mineralocorticoid excess appears to be the main driver of disease progression; however, it is not known whether individual differences in intra-arterial plasticity and effective sodium potassium exchange alter the overt clinical presentation. Here, we describe a patient with chronic hypokalemia and normal blood pressure with the diagnosis of a unilateral aldosterone-producing adenoma. Clinical Case A 47-year-old woman with no significant medical history was referred to endocrinology for evaluation of isolated hypokalemia since 2012. Her potassium was 2.8mEq/L at its lowest a month prior to her visit and had numerous other values less than 3.5mEq/L over the past 10 years. She did not carry a diagnosis of hypertension nor was she hypertensive at the time of her initial and subsequent evaluations. Results on initial endocrinology evaluation demonstrated a potassium of 3.2mEq/L (3.5-5.0mEq/L), Plasma Aldosterone Concentration (PAC) of 29ng/dL (≤21ng/dL), Plasma Renin Activity (PRA) of 0.42ng/mL/h (0.25-5.82ng/mL/h), and Aldosterone Renin Ratio (ARR) of 69. PA was suspected based on hypokalemia with an ARR &amp;gt;30 and PAC &amp;gt;20ng/dL. Further work-up was pursued to confirm the diagnosis as the patient did not have hypertension. She underwent 3-day oral sodium loading. 24-hour urine collection at the conclusion revealed adequate sodium loading with a urine sodium content of 208mEq/24hr (&amp;gt;200mEq/24hr) and aldosterone secretion of 41.3mcg/24hr (&amp;lt;12mcg/24hr). She subsequently underwent a CT abdomen demonstrating a 1.3×0.8 cm right adrenal nodule. Adrenal venous sampling was performed (continuous cosyntropin infusion with simultaneous adrenal venous sampling) which revealed a cortisol-corrected aldosterone lateralization ratio (right to left) of 406 at -5 minutes, 368 at 0 minutes, 33 at 10 minutes and 85 at 15 minutes. Results were consistent with strong lateralization to the right with contralateral suppression. Diagnosis of a right-sided aldosterone-producing adenoma was confirmed and she was referred to surgery for right adrenalectomy. Conclusion This case highlights one of the many presentations of PA. The persistent hypokalemia for a decade suggests a history of longstanding untreated PA prior to eventual diagnosis, yet the patient has remained normotensive. Though normotensive PA is a recognized entity, most patients develop hypertension within 5 years. The ability to remain normotensive despite intravascular volume expansion may highlight the patient's highly compliant vasculature and kidneys that have likely adapted to excrete high sodium loads in the setting of sodium excess. This case emphasizes that isolated hypokalemia in patients without hypertension should prompt consideration of PA and that patients with PA may maintain normotension for multiple years. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

PSAT219 Renal Phosphate Wasting Caused by ENPP-1 mutation.

Abstract Background Increased renal phosphate loss can be Fibroblast Growth Factor-23 (FGF-23) dependent or independent. FGF-23 reduces expression of Sodium-Phosphate co-transporters, responsible for phosphate reabsorption; and by inhibition of 1-alpha hydroxylation of 25-OH-D3. Reduced serum concentration of 1, 25-OH2-D3 results in secondary hyperparathyroidism. Ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) mutation is one of the rarest causes of hypophosphatemia, which causes FGF-23 dependent hypophosphatemia. Case description 31-year-old female referred to endocrinology for evaluation of recurrent nephrolithiasis despite normalization of PTH and serum Calcium (Ca) after right inferior parathyroid adenoma resection. Repeated renal stone analysis revealed calcium phosphate as the major stone composition. Patient achieved mid parental height, denied history of calcium or phosphate metabolism disorders/ rickets in the family. Physical exam was not suggestive of rickets and skeletal survey showed normal bone mineralization. Initial labs following parathyroid adenoma resection showed normal Ca 9.7 mg/dl, PTH 47 pg/ml, Phosphorus (Ph) 2.3 mg/dl, 25-OH-D3 51 ng/ml, albumin 3.9 g/dl, Mg 1.8 mg/dl. Repeat fasting labs six months later revealed Ca 9 mg/dl, Ph 1.7 mg/dl, 25-OH-D3 52 ng/ml, PTH 67.5 pg/ml and albumin 3.7 g/dl. Persistent low serum phosphate was evaluated further by a 24-hour urine collection which revealed high urine phosphate of 828 mg/day, Ca 181 mg/day, Mg 23 mg/day and creatinine was 1485 mg/day. Tubular reabsorption of phosphorus was 77% (normal: &amp;gt;80%), indicating renal phosphate wasting. Serum FGF-23 on two different days was &amp;gt;180 RU/ml. Next-generation sequencing tested positive for heterozygous ENPP-1 gene mutation variant c1441C&amp;gt;T (p. Arg481Trp). Patient was started on oral Phosphorus supplementation &amp; calcitriol. Repeat labs showed normalization of Ph 2.4 mg/dl. Audiology evaluation suggested mild sensorineural hearing loss. Heart calcium score was zero. Discussion ENPP1 gene mutation's clinical presentations can vary from no symptoms, hypophosphatemic rickets to death in the first six months of life from generalized arterial calcification. ENPP1 is an enzyme, which degrades ATP into adenosine monophosphate (AMP) and pyrophosphate (PPi). PPI is an inhibitor of hydroxyapatite crystallization in vascular tissue and organs, while Ph is a pro-mineralization factor. ENPP1 gene mutation results in a low concentration of PPi, predisposing the patient to pathological calcification. It is speculated that ENPP-1 modulates FGF-23 secretion. FGF-23 elevation in these patients is a protective response, as hypophosphatemia prevents pathological calcification. Treatment target is to keep phosphate at low end of normal. In our patient, ENPP- 1 mutation likely contributed to recurrent renal stones and possible parathyroid adenoma. Evaluation of genetic mutations is necessary to decide for or against FGF-23 antibody/Burosumab treatment. In ENPP-1 mutation. Burosumab should be avoided as it can bind to FGF-23 resulting in pathological calcification. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

OR21-5 Hypocalciuria is Common and Associated with Delayed Parathyroidectomy in Patients with Primary Hyperparathyroidism

Abstract Background A 24-hour urine collection is routinely obtained in the workup of primary hyperparathyroidism (PHPT) to measure calcium and creatinine excretion, rule out familial hypocalciuric hypercalcemia, and guide diagnosis and management. Although hypercalciuria is expected and frequently observed in PHPT, hypocalciuria and/or a low urine calcium (uCa) to creatinine clearance ratio (UCCCR) may occur. Variables including race, age, renal function, and 25-OH vitamin D levels can affect urinary calcium excretion. Given the utility of obtaining urine calcium excretion in patients with PHPT, we performed a retrospective analysis on patients with PHPT to evaluate the effect of clinical variables on urinary calcium excretion, and to test the hypothesis that hypocalciuria may delay parathyroidectomy in PHPT. Methods We retrospectively reviewed charts of patients with PHPT with available 24-hour uCa who underwent successful parathyroidectomy at our institution between 2009 and 2021. We extracted available demographic, clinical, and laboratory data including first available uCa and creatinine excretion prior to parathyroidectomy, age, gender, ethnicity, BMI, eGFR, serum calcium, phosphorus, PTH, 25-hydroxyvitamin D, and 24-hour sodium excretion. The association between these parameters and uCa and UCCR was assessed in univariate and multivariate models. We compared characteristics of PHPT patients with vs. without hypocalciuria, and duration between uCa measurement and parathyroidectomy. Results 643 PHPT patients were included in this analysis. 8.4% of patients had a 24-hr uCa excretion rate below 100mg/day, and 18.7% had a UCCR&amp;lt;1%.Compared to PHPT patients with UCCCR≥1%, those with UCCCR&amp;lt;1% had a significantly higher proportion of African Americans (22.2% vs 9.1%; p=0.0029), a lower mean serum calcium (p=0.0027), and 25-hydroxyvitamin D (p=0.035). In multivariate analysis, gender, race, serum calcium, serum 25-OH-vitamin D, and 24-hour urine sodium were all significant predictors of UCCCR. The UCCCR&amp;lt;1% group had a significantly longer median time from uCa measurement to parathyroidectomy [8.4 (Interquartile range IQR: 3.3-29.4) vs. 4.2 (IQR: 2.4-8.7) months, p&amp;lt;0.001).Compared to PHPT patients with 24-hr uCa≥100 mg/day, those with 24-hr uCa&amp;lt;100 mg/day had significantly lower mean serum calcium (p=0.002), eGFR (p&amp;lt;0.0001), urine sodium excretion (p=0.036), and significantly greater serum phosphorus (p=0.0085) and PTH (0.0078). In multivariate analysis, race, BMI, serum calcium, eGFR and urine sodium were all significant predictors of 24-hr uCa. The uCa&amp;lt;100 mg/day group had a significantly longer median time from uCa measurement to parathyroidectomy [9.7 (IQR: 3.3-32.2) vs. 4.2 (IQR: 2.4-8.8) months, p&amp;lt;0.001). Conclusions Although elevated uCa is used as a diagnostic marker and indication for parathyroidectomy in PHPT, hypocalciuria and UCCCR&amp;lt;1% are relatively common in PHPT patients, and associated with a significant delay in parathyroidectomy. Intrinsic (race, gender) and extrinsic (vitamin D status, renal function, sodium intake/excretion) factors are all determinants of calcium excretion in PHPT. Presentation: Monday, June 13, 2022 12:00 p.m. - 12:15 p.m.

PSAT046 Herbal Supplement Causing Cushing's Syndrome in a Patient With Severe Tophaecous Gout

Abstract Previous reports describe self-prescribed prolonged use of steroids resulting in Cushing Syndrome to treat tophaceous gout1,2. We present a case of Chinese herbal supplements used for severe tophaceous gout causing Cushing's syndrome. The patient is a 29-year-old male with prior history of severe tophaceous gout since age 18y, who presented to the hospital for fatigue and episodes of lightheadedness associated with shortness of breath and melena over the past four months. On physical examination, he had moon facies, central obesity, purple striae in the abdominal wall and axillary region, and large, deforming tophi in bilateral elbows and toes. He reported using a Chinese herbal supplement of unknown contents for the past year to maintain his gout attacks under minimal control. Admission hemoglobin was 4.2 mg/dL with severe iron deficiency. Due to suspected gastrointestinal bleed, he underwent work-up with EGD and colonoscopy, which did not reveal a bleeding source. His hemoglobin stabilized after four red blood cell transfusions with plans to do a video capsule outpatient. His celiac disease work-up was negative. Due to persistent fever and tachycardia, infection was ruled out with negative COVID PCR, viral panel, and QuantiFERON test. Work-up for suspected Cushing's syndrome showed ACTH level &amp;lt; 3 pg/mL (7-84 pg/mL), morning cortisol 10 mg/dL (5-20 mg/dL), and DHEA sulfate 21.6mg/dL (160-449 mg/dL). Subsequent 24-hour urine collection showed elevated free cortisol at 127 µg/24hr (£60 µg/24hr) with ratio 101 µg/g Cr (&amp;lt; 32 µg/g Cr). It was suspected that the Chinese herbal supplement had high contents of synthetic steroids as previously reported in literature2 with resultant development of exogenous Cushing syndrome. He reported not taking his herbal supplement for a couple of days before admission; therefore, he was treated with high-dose steroids for suspected acute gout flare with resolution of his tachycardia and fever after completing testing for Cushing Syndrome. No further episodes of melena were reported, and his hemoglobin remained stable. He was discharged with steroid taper over eight weeks and planned a Cortrosyn test when the steroid dose is 5 mg before discontinuing treatment. Chinese herbal supplements can contain synthetic steroids, and unsupervised use can lead to adverse effects like Cushing's syndrome, as reported in our patient. 1. Lo TEN, Racaza GZ, Penserga EG. "Golden Kernels within the skin": disseminated cutaneous gout. Case Reports 2013; 2013. 2. Edwards CJ, Lian TY, Chng HH. Cushing's syndrome caused by treatment of gout with traditional Chinese medicine. QJM 2002; 95: 705–705. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

ODP130 Zoledronate-Induced Acute Tubular Necrosis With Baseline Normal Renal Function: A Rare Phenomenon

Abstract Introduction Zoledronate is an intravenous bisphosphonate that is commonly used to decrease bone resorption in patients with osteoporosis. The incidence of acute tubular necrosis (ATN) using zoledronate in patients with normal renal function is rare. Herein, we report the occurrence of severe ATN following treatment with a single zoledronate infusion in a patient with osteoporosis and normal renal function. Case Presentation A 51-year-old female with hypertension, well-controlled type 2 diabetes c/b gastroparesis without nephropathy(HbA1c6.8%), status-post hysterectomy, and bilateral oophorectomy, who was recently diagnosed with osteoporosis. Bone densitometry with Hologic revealed T scores of -2.8 at the spine and a T score of - 0.9 at the left hip. Her medications included lisinopril, metformin, and empagliflozin. Due to a history of gastroparesis, zoledronate was chosen as the preferred treatment. Pre-infusion blood work showed: a creatinine of 0.92 (0.5-1.1 mg/dl), 25-hydroxyvitamin-D 37.8 (30-100 NG/ml), calcium 8.9 (8.5-10.5mg/dl) and urine microalbumin 14 (&amp;lt;30 mg/g). Two days after the infusion, the patient developed emesis, diarrhea, oliguria, and fevers. She was evaluated in the emergency room and found to have acute renal failure (creatinine 10 mg/dL). She was given three liters of intravenous fluids with no improvement in urine output. Microscopic evaluation of spun urine revealed non-dysmorphic RBCs and numerous muddy brown granular casts consistent with ATN. Despite treatment with intravenous fluids, her creatinine did not improve and peaked on hospital days 11 to 11.65mg/dl. A 24-hour urine collection revealed proteinuria of 3 grams/24 hours. The patient was then empirically started on methylprednisolone 500mg for suspected glomerulonephritis. A renal biopsy was subsequently performed, which confirmed ATN. The patient's creatinine improved steadily to 5.49mg/dl by discharge. A subsequent creatinine one-month post-discharge was 1.36mg/dL. Discussion Zoledronate is widely used at low doses in the treatment of osteoporosis. ATN due to zoledronate infusion has been described in patients with pre-existing renal dysfunction and those receiving large and frequent doses for malignancy but rarely reported with the lower doses used to treat patients with osteoporosis and normal renal function. Zoledronate is believed to cause ATN by internalization in the renal tubular cells via the process of fluid-phase endocytosis. The intracellular accumulation of zoledronate may act as an epithelial toxin inducing tubular cytotoxicity. Interestingly, our patient had normal renal function without diabetic nephropathy and did not use nephrotoxic medications prior to the infusion. Conclusion We report a case of severe ATN due to a single dose of zoledronate in a patient with osteoporosis and previously normal renal function. This case highlights the need to be aware of the potential nephrotoxicity of zoledronate even in patients with normal renal function at baseline. Presentation: No date and time listed

Paralysis Due to Hypokalemia and Hypocalcemia: A Case Report

Background&#x0D; Hypokalemia is the most frequent electrolyte disorder encountered in clinical practice. It caused by inadequate potassium intake or excessive renal or gastrointestinal potassium loss. Hypokalemia may associate with muscle weakness. Hypocalcemia can result from disorders of vitamin D metabolism and action, hypoparathyroidism, resistance to parathyroid hormone (PTH), or other conditions such as nutritional deficiency. Numbness and tingling sensation may occur on hypocalcemia.&#x0D; Case presentation &#x0D; A 36-year-old woman came with complaints of weakness of upper and lower limbs three days before admission. At first, the weakness felt suddenly on the left arm and left foot after waking up in the morning, making her not being able to walk. Patient felt tingling sensation on her face, upper limbs, and lower limbs. Her hands felt stiff as well as her mouth. Patient had a decreasing serum level (3 mEq/l) and decreasing total calcium level (4,8 mg/dL).&#x0D; Conclusion&#x0D; In young adult patients with limbs weakness, it is necessary to consider electrolyte imbalance, such as hypokalemia and hypocalcemia. Hypokalemia can be caused by decreased potassium intake, excessive vomiting, drug consumption, kidney disease, and endocrine disease. To diagnose hypokalemia, it is necessary to carry out further examinations such as basic biochemical laboratories (magnesium, calcium, phosphorus), blood gas analysis, TSHs, urine analysis (urine calcium, potassium excretion in 24-hour urine collection), drug screening.&#x0D;

Association between nocturnal blood pressure dipping and chronic kidney disease

Abstract Introduction Management of blood pressure (BP) in chronic kidney disease (CKD) is critical for preventing cardio-renal complications. While increasing attention has been given to discrepancies between office and ambulatory BP control in this population, information on nocturnal BP decrease patterns (dipping) in CKD is still scarce. Purpose We aimed at describing nocturnal BP dipping patterns and its predictors in patients with CKD. Methods We analysed data from patients with CKD stages 1 to 5 referred for kidney function testing from September 2006 to January 2022, including 24-hour urine collection, gold-standard measurement of glomerular filtration rate (GFR) using clearance of a radioisotopic tracer, as well as ambulatory BP measurement (ABPM) in a single tertiary hospital in Paris, France. A total of 1177 ABPM were available in 642 participants. The magnitude of dipping was calculated as the difference between day- and night-time systolic BP (SBP), in percentage of daytime SBP. Participants were then categorized as extreme-dippers (≥20%), dippers (10% to &amp;lt;20%), non-dippers (0% to &amp;lt;10%), or reverse-dippers (&amp;lt;0%). Factors associated with a less than 10% dipping were analysed with crude and adjusted logistic regression models including a random intercept to deal with clustering of measurements within patients. Results Participants (mean age 56±15 years; 35% female, mean GFR 49±21 mL/min per 1.73 m2) consisted of 8% extreme-dippers, 37% dippers, 40% non-dippers, and 15% reverse-dippers. The prevalence of non- or reverse-dipping increased with CKD severity, from 36% in CKD stage 1 to 65% in CKD stages 4–5 (Figure). In crude analyses, African origin, a lower measured GFR, a higher daytime SBP, diabetes, a higher number of antihypertensive medications and a higher 24-hour urinary sodium to potassium ratio (24h Na/K) were associated with abnormal dipping status. In the multivariable adjusted regression, non or reverse dipping was independently associated with measured GFR (odds ratio [OR, 95% confidence interval] per 10 ml/min/1.73 m2 decrease = 1.16 [1.06–1.26], p=0.001), daytime ambulatory SBP (OR per 10 mmHg decrease = 1.17 [1.06–1.28], p=0.001), African origin (OR= 1.56 [1.04–2.34], p=0.03) and 24h Na/K (OR per 1-unit increase = 1.20 [1.06–1.37], p=0.006). Conclusions The prevalence of nocturnal non-or reverse dipping BP profiles increases substantially across the spectrum of CKD. Measured GFR, ambulatory daytime SBP, African origin and 24-hour urinary sodium to potassium ratio are independent predictors of abnormal nocturnal BP decrease and thus may help in cardiovascular risk stratification in this population. More research is needed on whether nocturnal dipping may be a treatment target to reduce cardiorenal complications. Funding Acknowledgement Type of funding sources: None.

The Role of Urinary Potassium Examination on the Progressivity of Chronic Kidney Disease: A Narrative Literature Review

Kidneys play an important role in potassium homeostasis. The important role of the kidneys in maintaining potassium balance is reflected in the high level of potassium disturbances in patients with decreased kidney function, especially patients with severely decreased renal function and patients who have comorbidities, such as diabetes, hypertension, or heart failure. Chronic kidney disease is characterized by abnormalities of kidney structure or function that persist for more than 3 months, have many complex causes, and have a major impact on global health status. There are several methods to measure the amount of potassium intake consumed, including a food frequency questionnaire, dietary recall, temporary urine potassium examination, and 24-hour urine potassium examination. The standard gold measurement for evaluating urinary potassium excretion is through 24-hour urine collection. This literature review aims to describe the role of urinary potassium excretion in assessing the progression of chronic kidney disease.

Tubular Secretion and Estimated GFR Decline in the Jackson Heart Study

Secretion of solutes by the proximal tubules represents an intrinsic kidney function not directly reflected by the glomerular filtration rate (GFR). The early loss of secretory clearance may reflect unrecognized kidney dysfunction, portending future disease progression. We designed a nested case-control study within the Jackson Heart Study (JHS), a prospective study of African American adults in Mississippi, to associate baseline differences in proximal tubular secretion of 5 endogenously produced solutes with future estimated glomerular rate (eGFR) decline. We matched 127 pairs by creatinine-eGFR, age, diabetes, and sex among the patients who provided a 24-hour urine collection; cases had a ≥25% decline in eGFR compared to<10% in controls over 10 years of follow-up. We measured baseline plasma and urine concentrations of secretory solutes using liquid chromatography-mass spectrometry to determine the odds ratio of kidney disease progression. Mean age was 60 years; 76% were women; 30% had diabetes; mean baseline eGFR was 94±20 ml/min per 1.73 m2. The eGFR decline over 10 years was 38±13% in cases and 0±10% in controls. After adjustment for the matching variables plus albuminuria, systolic blood pressure, body mass index, and smoking, each 50% lower kidney clearance of isovalerylglycine, kynurenic acid, and xanthosine were associated with 1.4 to 2.2 greater odds of eGFR decline. Kynurenic acid exhibited the strongest association; each 50% lower clearance of this secretory solute was associated with 2.20-fold higher odds of eGFR decline (95% confidence interval [CI] 1.32-3.67). We found that in this community-based study of adults without significant kidney disease, lower proximal tubular secretory solute clearance is associated with future eGFR decline.

Comparison of three spot urine formulae and their validation using 24-hour urine sodium for estimation of daily salt intake: a cross-sectional study among Bangladeshi adults

ObjectiveThis study aimed to assess the validity of three commonly used (Tanaka, Kawasaki, INTERSALT) methods based on spot urinary sodium excretion against the 24-hour urinary sodium excretion to estimate the...

423.12: Dietary Protein Intake and Blood Pressure After Living Kidney Donation

Background: High dietary protein intake is associated with worsening kidney function especially in at-risk patients such as living kidney donors; high blood pressure is a known risk factor for kidney disease. Whether pre-donation protein intake contributes to post-donation blood pressure is unknown. Methods: A single-center cohort study included living kidney donors undergoing living kidney donation in 2021 and divided the patients into 2 groups: low and high pre-donation protein intake defined by dietary protein intake estimated from 24-hour urine collection <1 (LPI) and ≥1 (HPI) g/kg/day, respectively. Association between dietary protein intake and systolic blood pressure during the first two weeks post-donation was evaluated by multiple linear regression. Results: Of 14 living kidney donors, mean±SD was 44±12 and 50% were female. Half of the study population were in the LPI group with a mean dietary protein intake of 0.8±0.1 g/kg/day and the remaining seven patients in the HPI group had a dietary protein intake of 2.2±2.5 g/kg/day (meandifference HPI vs LPI 1.4; p 0.172; 95%CI -0.7, 3.5). Dietary sodium intake was not different between the two groups (mean sodium intake of LPI 3,171±1,315 and of HPI 4,058±1,135 g/day, meandifferenc HPI vs LPI 887; p 0.202; 95%CI -544, 2,318; Figure 1). Mean systolic blood pressure of LPI and HPI groups were 135±8 and 121±7 mmHg, respectively (meandifference LPI vs HPI 14; p 0.007; 95%CI 5, 23). Compared to the LPI group, the HPI group had 14 mmHg lower systolic blood pressure (β -14; p 0.007; 95%CI -23, -5; Figure 2). After adjusted by age, gender, ethnicity, pre-donation body mass index, dietary sodium intake (<4 vs ≥4 g/day), and the interaction term between dietary protein intake and dietary sodium intake, the magnitude and direction of the association between dietary protein intake and systolic blood pressure remain the same (β -13, p 0.043, 95%CI -26, -0.6) and dietary sodium intake did not modify the association (Pinteraction 0.498). Conclusions: Higher dietary protein intake during pre-donation is inversely associated with SBP level without the effect of dietary sodium intake. Although HPI is associated with adverse kidney outcomes, the protective association between HPI and high blood pressure may involve physiological change after donor nephrectomy and further studies with long-term follow-up are required.

Excretion of oxidated cortisol metabolites is markedly lower than previously assumed: An analysis of urinary cortoic acids in healthy children by GC–MS

Discovered about 50 years ago, the four C21 steroidal acids (α-)cortolic acid, β-cortolic acid, (α‑)cortolonic acid and β-cortolonic acid present the oxidative end products of cortisol metabolism. Undergoing renal elimination, these cortoic acids have been assumed to constitute up to 25 % of total urinary cortisol metabolites. However, their analysis has been difficult, only few data has been published in adults, and this class of steroids has become practically forgotten. Since data in children are lacking and nothing is known about their metabolism during human development, we aimed at establishing a more practical analytical method and determined their urinary concentrations in a high number of healthy subjects. In our method, 5-mL-aliquots of 24-hour urine samples were subjected to solid phase extraction (C18 cartridges), followed by strong anion exchange chromatography, and formation of 2-propylester-trimethylsilylether derivatives (2-PR/TMS). The cortoic acids were quantified by targeted gas chromatography–mass spectrometry (GC–MS) using a nonpolar GC column and selected ion monitoring (SIM). Baseline separation of all cortoic acids was achieved. Calibration graphs were linear (R2 > 0.98). Variations in precision and accuracy were less than 15 %, respectively. The detection limit was 100 pg (injected) with a signal-to-noise ratio of 3. 240 specimens from 24-hour urine collections from healthy children (120 boys, 120 girls, aged 3–18 years; DONALD study) were analyzed for cortoic acids and neutral cortisol metabolites to create first reference ranges. The profile of cortoic acids was dominated by α-cortolonic acid with excretion rates up to 70 µg/d. Absolute excretion rates of cortoic acids increased with age, their total excretion rates ranged between 11.0 and 127.3 µg/d (median 45.7 µg/d), but did not show any sexual dimorphism. Since cortoic acids make up only about 1 % of total urinary cortisol metabolites, determination of neutral urinary steroids reliably allows assessment of cortisol production. However, cortoic acids might present potential biomarkers of the body’s redox state.

Interference of preservatives on urinary iodine measurement by Sandell–Kolthoff method

This report aimed to determine the effects of different preservatives used to maintain the integrity of urine samples for a 24-hour urine collection on urinary iodine measurement by the Sandell–Kolthoff method in vitro. The selected preservatives were hydrochloric acid, acetic acid, boric acid, sodium carbonate, sodium fluoride, thymol with isopropanol, sodium chloride with formalin, and Saccomanno fixative. The test samples to which these preservatives were added and the control samples for basal measurements were prepared from the urine pool obtained from urine samples taken from healthy volunteers. The urinary iodine measurements were performed following the calculated minimum number of replicates in these prepared samples. The data analysis of the interferences of the preservatives was performed based on the Clinical and Laboratory Standards Institute EP7-A2 guideline. The preservatives that had more acceptable effects on the urinary iodine measurement compared to the others were sodium carbonate (0.5% w/v) and thymol (10% w/v) with isopropanol (0.25% v/v) for 24-hour storage at room temperature. This report presented reliable and usable data revealing the effects of preservatives, which are frequently used to maintain the integrity of urine samples for a 24-hour urine collection, on urinary iodine measurement. There are need to reveal the possible effects of potential exogenous interfering substances and the pathological levels of endogenous analytes or shaped elements in the urine matrix on methods with routine clinical use in making medical decisions.