Urinary Calcium-creatinine Ratio Research Articles

Daily versus fortnightly oral vitamin D3 in treatment of symptomatic vitamin D deficiency in children aged 1-10 years: An open labelled randomized controlled trial.

Compare the efficacy and safety of daily versus fortnightly oral vitamin D3 in treating symptomatic vitamin D deficiency in children aged 1-10 years. Open labelled randomized controlled trial. Eighty children with symptomatic vitamin D deficiency were randomized into group daily (D) and group bolus (B) [40 in each group] to receive oral vitamin D3, 4000 IU daily or 60,000 IU fortnightly for 12 weeks respectively. Both groups received daily oral calcium of 500 mg/day. Serum calcium (Ca), phosphate (P), alkaline phosphatase (ALP), 25-hydroxy cholecalciferol (25(OH)D), parathyroid hormone (PTH) levels, urine calcium: creatinine ratio and radiological score were assessed at baseline, 4 weeks and 12 weeks. At the end of 12 weeks, 74 children were available for evaluation of the efficacy and safety of both regimens. Both regimens led to a significant increase in Ca and P levels and a fall in ALP and PTH levels from baseline to 4 and 12 weeks of therapy, with no intergroup difference. At 4- and 12-week assessments, all children in both treatment arms achieved 25(OH)D level in sufficiency range,with no significant difference in their geometric mean. Both regimens were associated with asymptomatic transient hypercalcemia [group D-51.4% vs. group B-34.3%; p-0.14] and hypercalciuria (5.7%) in group D that resolved spontaneously on follow-up. Daily and fortnightly oral vitamin D3 in similar cumulative doses are efficacious for treating symptomatic vitamin D deficiency in children (1-10 years). Treated children should be monitored for serum 25(OH)D, Ca and urinary calcium creatinine ratio.

P-11 Case report of Primary Hyperparathyroidism and Pulmonary Embolism

Abstract Introduction Primary hyperparathyroidism (PHPT) is a disorder characterized by excessive parathyroid hormone secretion, resulting in hypercalcaemia. Patients with PHPT are believed to be in a hypercoagulable state due to the role of calcium in the platelet function and the coagulation pathway. Clinical Case An 82-year-old male with a background history of deep vein thrombosis twelve years ago, was admitted with left leg pain following a fall, he was found to have an intra-capsular left neck of femur fracture for which he underwent left hip hemiarthroplasty at a later stage during his admission. He was also found to have adjusted calcium of 2.9 mmol/L at admission, parathyroid hormone of 15.2 pmol/L, raised urine calcium-creatinine ratio of 0.39 and he was vitamin D replete (vitamin D 50.3 nmol/L). He was treated for delirium and a urinary tract infection and his inflammatory markers continued to worsen, this triggered performing a CT scan of the chest, abdomen and pelvis, which revealed a right parathyroid nodule and an acute pulmonary embolism (PE). He was commenced on prophylactic dose of low molecular weight heparin at admission, it was changed to a therapeutic dose of low molecular weight heparin after the PE diagnosis and then to Apixaban for three months. The patient was assessed to not be suitable for parathyroidectomy, the decision was made to manage the PHPT medically and he is going to be followed up locally at the Endocrinology Clinic. Conclusion There have been few case reports suggesting a correlation between the hypercalcaemic PHPT and the risk of venous thromboembolism. Ionised calcium is necessary for thrombin formation, platelet activation and aggregation, as well as activation of various clotting factors, such as factor VII and factor X. Studies have also shown that these patients have increased protein S activity and fibrinogen levels. This case, among other cases that we have observed in our hospital, highlights that the hypercalcaemia could pose an additional hypercoagulability risk in the presence of other risk factors.

Urinary Calcium Creatinine Ratio and Association with Pre-Eclampsia

Urinary Calcium Creatinine Ratio and Association with Pre-Eclampsia

Study protocol for supplementation of single high dose Vitamin D in deficient critically ill children and assessment of their short-term outcome: An open label randomized control trial

Vitamin D is a fat-soluble vitamin and is classically considered to play a major role in bone metabolism and maintaining Calcium and phosphorus equilibrium. With progressing research, other roles of Vitamin D are surfacing. The pleotropic functions of Vitamin D regulate cell proliferation, differentiation, apoptosis, and angiogenesis. In critically ill children, Vitamin D deficiency is associated with poor outcomes in the form of increased PICU stay, increased duration of mechanical ventilation, higher rate of Ventilator Associated Pneumonias, increased incidence of sepsis, higher intensive care scores and increased incidence of end organ dysfunction. With this background, we aim to conduct an open label Randomized Control Trial to study the short-term outcome of Vitamin D deficient critically ill children after supplementation of a single high dose oral Vitamin D. This will be an open label randomized control trial conducted at a tertiary care hospital in central India. Children aged 1 month to 18 years, admitted in the pediatric intensive care unit with Serum Vitamin D level less than 20 ng/dL will be the study group. These children will be randomized into two groups as per the computer-generated randomization. Group A will receive standard treatment protocol with 10,000 IU/Kg to 400,000 IU (maximum) Vitamin D via mouth or nasogastric tube, whereas Group B will receive standard treatment protocol. Urinary calcium-creatinine ratio will be done on day 3 in Group A to check for hypervitaminosis D. The outcome of both the groups will be assessed. All the data will be added to a Microsoft Excel sheet. Results and interpretation will be determined on the basis of the obtained observation. Trial registration: CTRI/2022/10/046556.

Urinary calcium creatinine ratio in breast fed and artificial fed healthy infants

Urinary calcium creatinine ratio in breast fed and artificial fed healthy infants

Burosumab for X-linked hypophosphatemia in children and adolescents: Opinion based on early experience in seven European countries.

Given the relatively recent introduction of burosumab in the management of X-linked hypophosphatemia (XLH), there is limited real-world data to guide its use in clinical practice. As a group of European physicians experienced with burosumab treatment in clinical practice, we convened with the objective of sharing these practice-based insights on the use of burosumab in children and adolescents with XLH. We attended two virtual meetings, then discussed key questions via Within3, a virtual online platform. Points of discussion related to patient selection criteria, burosumab starting dose, dose titration and treatment monitoring. Our discussions revealed that criteria for selecting children with XLH varied across Europe from all children above 1 year to only children with overt rickets despite conventional treatment being eligible. We initiated burosumab dosing according to guidance in the Summary of Product Characteristics, an international consensus statement from 2019 and local country guidelines. Dose titration was primarily guided by serum phosphate levels, with some centers also using the ratio of tubular maximum reabsorption of phosphate to glomerular filtration rate (TmP/GFR). We monitored response to burosumab treatment clinically (growth, deformities, bone pain and physical functioning), radiologically (rickets and deformities) and biochemically (serum phosphate, alkaline phosphatase, 1,25-dihydroxyvitamin D, 25-hydroxyvitamin D, urine calcium-creatinine ratio and TmP/GFR). Key suggestions made by our group were initiation of burosumab treatment in children as early as possible, from the age of 1 year, particularly in those with profound rickets, and a need for clinical studies on continuation of burosumab throughout adolescence and into adulthood.

Effects of lemon-tomato juice consumption on crystal formation in the urine of patients with calcium oxalate stones: A randomized crossover clinical trial.

Dietary supplementation with citrate-containing juices may serve as an effective alternative to potassium citrate therapy for preventing calcium oxalate stone recurrence. This study was performed to evaluate whether consumption of lemon-tomato juice can decrease the tendency for stone formation in the urine of calcium oxalate stone formers. The study was conducted as a prospective interventional randomized crossover clinical trial with a repeated-measures design. Twenty-two patients with calcium oxalate stones and no metabolic abnormalities in the urine treated with lithotripsy at a tertiary care center from August 2017 to July 2018 were recruited. After a 14-hour overnight fasting, urine samples were collected after the patients consumed either milk only or milk and lemon-tomato juice. Their urine was tested for multiple parameters, including urine pH, specific gravity, calcium-creatinine ratio, and supersaturation with sodium oxalate, followed by optical density measurement via spectrophotometry. There were no significant differences in the background characteristics between the 2 groups. The optical density of the urine samples obtained after consumption of milk only was significantly higher than that after consumption of milk and lemon-tomato juice (mean = 0.131 for milk only vs. 0.053 for milk and lemon-tomato juice, p < 0.001). The urine calcium-creatinine ratio was similar between the groups (mean = 0.141 for milk only vs. 0.076 for milk and lemon-tomato juice, p = 0.019). The addition of lemon-tomato juice as a source of citrate in the diet significantly decreases the established risk factors for calcium oxalate stone formation in patients. This study was prospectively registered at CTRI under number CTRI/2017/04/008312 on April 7, 2017.

Effect of deferasirox on renal function in thalassemic children

Abstract Background: Iron-chelating therapy causes improvement in the life expectancy of thalassemic patients. Deferasirox (DFX) is an oral iron chelator with an established dose-dependent efficacy, though alteration of renal function has been observed in many studies. In the present study, we evaluated the effect of treatment with DFX on renal function. Materials and Methods: This quasi-experimental study was done in the Thalassemia Center of Bangladesh Shishu Hospital and Institute from June 2019 to July 2021, where 50 thalassemia major and E-β thalassemia children aged 2–18 years old were included. Blood urea nitrogen (BUN), serum creatinine, spot urinary protein creatinine ratio, spot urinary calcium creatinine ratio, and estimated glomerular filtration rate (eGFR) were measured. If renal functions were normal, DFX was started at a dose of 25 mg/kg/day. After 6 months of DFX treatment, the abovementioned investigations were repeated and analysis was done. The study variables were analyzed by paired t-test. P value &lt;0.05 was considered significant. Results: The mean age of the thalassemic children was 5.21 ± 1.72 years. Before treatment, mean serum creatinine was 39.78 ± 3.12 μmol/L, and after 6 months, serum creatinine was increased but not statistically significant. The mean value was 40.50 ± 3.39 μmol/L after 6 months (P value 0.071). There was no significant change of BUN. Initially, the mean BUN was 3.39 ± 0.76 mmol/L, and 6 months after treatment, it was 3.45 ± 0.70 mmol/L. Initially, the spot urinary protein creatinine ratio was 0.12 ± 0.04, and after 6 months, the mean value was 0.43 ± 0.24. it was significantly increased (P value &lt;0.001). Initially, the spot urinary calcium creatinine ratio was 0.068 ± 0.043, and after treatment, it was significantly raised. The mean value was 0.191 ± 0.168 (P value &lt;0.001). After 6 months of treatment with DFX, 35 patients developed mild proteinuria, and eight patients developed hypercalciuria. There was no significant change of eGFR before and after treatment. Conclusions: In this study, we got significant proteinuria and hypercalciuria but nonsignificant changes in serum creatinine, BUN, and eGFR.

ODP564 Hypercalcemia in the Setting of HTLV-1 Infection and Normal PTHrP Levels

Abstract A 53 year old male with history of HTLV-1 infection associated myelopathy but with unknown mode of transmission, presented with acute on chronic bilateral lower extremity weakness and numbness with no other deficits. Examination revealed decreased strength (grade 1/5) in lower extremities with normal bulk, tone and sensations. Initial blood work revealed hypercalcemia with corrected Calcium of 16.2mg/dl(8.5-11.5), Phosphorus of 2.7mg/dl (2.5- 4.5) and Alkaline Phosphatase of 126mg/dl(20-140). Workup for hypercalcemia revealed Parathyroid hormone (PTH) level of 14pg/ml (10-65), 25 hydroxy vitamin D at 19.6 ng/ml(30-100), 1,25 dihydroxy vitamin D at 6.7pg/ml(19.9-79.3) and TSH of 1.265 microIU/ml(0.5-5). The Parathyroid hormone related protein(PTHrP) level was low at &amp;lt; 2pmol/L while Lactate Dehydrogenase (LDH) was 433U/L(100-220). Urine calcium creatinine ratio was 0.388. Reverse Transcriptase PCR was positive for HTLV-1 but negative for HTLV-2. Smudge cells and atypical lymphocytes were noted on peripheral smear. Imaging revealed generalized lymphadenopathy with splenomegaly but no spinal cord compression. Flow cytometry showed 7.8% atypical helper T cells, positive for CD3, CD4, CD5 and CD45. Clonal T cell receptor gene rearrangements were found, suggesting an underlying T cell neoplasm. Lymph node biopsy confirmed ATLL. He received treatment with fluids, Calcitonin and Denosumab after which serum Calcium levels fell (nadir 7.7mg/dl) and then normalized. He developed another episode of hypercalcemia 5 weeks later which was treated similarly. Discussion Human T cell Lymphotropic Virus-1 (HTLV-1) is a retrovirus causing asymptomatic infections, symptomatic systemic disorders and adult T cell Leukemia and lymphoma(ATLL). HTLV-1 infections, whether in asymptomatic or symptomatic patients, and ATLL are rare but important causes of hypercalcemia and hypercalcemic crises. Individuals with ATLL have the highest incidence of hypercalcemia(50-70%) among all hematologic malignancies. Hypercalcemia is a poor prognostic factor and predicts lower overall survival. It is caused by increased bone resorption, mediated by various factors with the largest role being played by Receptor Activator of Nuclear Factor Kappa B ligand (RANKL), followed by PTHrP, Interleukins, Macrophage Inflammatory Protein 1 alpha and gp 46. RANKL expression is increased upon transactivation by the viral TAX gene product and mediates conversion of osteoclast precursors to mature osteoclasts engaging in bone resorption. PTHrP expression is variable among patients, relating to levels of the TAX gene product that transactivates the PTHrP gene promoter. Thus, a low level, like in our patient, does not rule out HTLV infection as the cause of hypercalcemia. Management of hypercalcemia is in keeping with guidelines for management of other causes of hypercalcemia but may be better responsive to monoclonal antibodies against RANKL than bisphosphonates given the role of the ligand in mediating hypercalcemia in these cases. It can also be used in the setting of poor renal function, which is commonly encountered in hypercalcemic patients. Presentation: No date and time listed

LBODP018 Hypercalcemia In A Child On Ketogenic Diet For Intractable Epilepsy

Abstract Introduction Ketogenic diets have been shown to significantly reduce seizures in patients with intractable epilepsy refractory to common antiepileptic medications. There have been reports of hypercalcemia in diet-controlled epilepsy patients. The exact cause of hypercalcemia in ketogenic diets is unclear but decreased bone formation and impaired calcium excretion are suggested mechanisms. Case An 8-year-old male with Lennox-Gastaut syndrome was noted to have incidental hypercalcemia on admission (serum calcium 11.5 mg/dL, n = 8.8-10.1) for aspiration pneumonia, UTI, and increased seizure-like activity. Hypercalcemia persisted throughout his hospitalization (range: 10.8-12.4 mg/dL). Evaluation of hypercalcemia indicated normal serum phosphate (5.6 mg/dL, n = 3. 0-6. 0), appropriately low PTH (9.5 pg/mL, n = 10. 0-65. 0), undetectable PTHrP (&amp;lt;2. 0 pmol/L), low 25 (OH) vitamin D (19ng/ml, n=30-100), low 1,25 (OH)2 vitamin D (7.1 pg/mL, n = 19.9-79.3), normal creatinine (0.3 mg/dL, n = 0.31-0.61), slightly elevated TSH (5.13 mIU/L, n = 0.5-4.5) with a normal free T4 (1.4 ng/dL, n = 0.8-2. 0), and physiologic CBC. Alkaline phosphatase was low (88 U/L, n = 156-386) and skeletal survey showed diffuse demineralization. Urine calcium creatinine ratio was elevated at 0.6 when serum calcium was 11.6 mg/dl. Patient was 7 months into a ketogenic diet that successfully reduced seizure frequency and the plan was to further intensify the diet. On hospital day 11 when serum calcium was 12mg/dl, he was started on IV normal saline and furosemide up to a daily dose of 60 mg. On hospital day 12, patient was started on calcitonin (3 U/kg twice daily SQ). Serum calcium normalized (10 mg/dl), but calcitonin had to be discontinued due to severe nausea and vomiting. GI symptoms did not improve on a lower calcitonin dose. Calcium gradually corrected on fluids and furosemide, but hypercalcemia recurred (11mg/dl) after furosemide was weaned. The patient was then transferred to a higher level of neurologic care to continue treatment and increase the intensity of the ketogenic diet. There, on cumulative hospital day 26, he received zoledronic acid (0. 0125 mg/kg) which was tolerated well and resulted in normalization of the serum calcium levels (10.9mg/dl, 10.2mg/dl and 9.8mg/dl on days 26, 28 and 29 respectively). Conclusions This case adds to the limited literature available on the evidence that management of refractory epilepsy with ketogenic diets may cause acute hypercalcemia. Although the underlying cause is unclear, decreased osteogenesis as marked by low alkaline phosphatase activity remains the likely explanation. Other risk factors such as immobilization also need to be explored. The successful implementation of protocols used to treat our patient and similar patients in the literature may help create screening protocols for early detection and management of the hypercalcemia to prevent complications. Presentation: No date and time listed

Evaluation of Urinary Calcium–Creatinine Ratio for Early Prediction of Preeclampsia

Background: Preeclampsia (PE) is one of the most important hypertensive disorders in pregnancy. It is one of the fatal complications with significant mortality and morbidity. Incidence of preeclampsia is around 5-10% of all pregnancies, and in developing countries like Bangladesh it is around 4-18%. Objective: The objective of this study was to determine the efficacy of urinary calcium-creatinine ratio in a spot urine sample for early prediction of preeclampsia in pregnant women. Methods: It's a cross sectional type of analytical study, done in the department of Obstetrics &amp; Gynaecology, Sir Salimuilah Medical College Mitford Hospital, Dhaka. After fulfilling inclusion and exclusion criteria total 100 pregnant women with risk factors of preeclampsia were enrolled as the study population. Results: Among different parameters serum calcium concentration of normal pregnancy and preeclampsia group varied significantly (p&lt;0.05). Women with preeclampsia showed reduced excretion of calcium in comparison to normal pregnant women when spot urinary calcium concentration was evaluated. In this study comparison of spot urinary calcium-creatinine ratio in normal pregnant woman and in preeclamptic women was done and the result was highly significant (p &lt;0.001). Conclusion: This study is intended to identify at risk patients and put selection criteria for primary prevention to reduce morbidity and mortality in patients of preeclampsia. It showed lower urinary calcium excretion and calcium-creatinine ratio in preeclamptic women than normotensive pregnant women. Therefore, a single random urinary calcium-creatinine may be an effective tool for the early diagnosis of preeclampsia.

Study the Correlation of Urinary Calcium-Creatinine Ratio as a Predictor of Pre-Eclampsia

Study the Correlation of Urinary Calcium-Creatinine Ratio as a Predictor of Pre-Eclampsia

Urine Calcium-Creatinine Ratio in Prediction of Pre-eclampsia.

Hypertensive disorders of pregnancy are first identified during pregnancy (gestational hypertension, pre-eclampsia, eclampsia, and HELLP syndrome) or may present as a complication of previously existing disease (chronic hypertension, renal disease, and systemic disease). These hypertensive disorders complicate the pregnancy, leading to significant maternal and perinatal morbidity and mortality, especially in low- and middle-income countries (Chappell in Lancet 398(10297):341-354, 2021). These hypertensive disorders are about 5-10% of all pregnancies. This is a single institutional study, which was conducted among 100 normotensive asymptomatic antenatal women at, 20-28weeks of gestation attending our OPD. Voluntary participants were selected based on inclusion and exclusion criteria. Spot urine sample was taken for estimation of UCCR by an enzymatic colorimetric method. These patients were followed up throughout the pregnancy and monitored for the development of pre-eclampsia. UCCR is compared in both groups. Pre-eclampsia women were further followed up to observe the perinatal outcomes. Among 100 antenatal women, 25 of them developed pre-eclampsia. UCCR of < 0.04 was considered as cutoff and compared between pre-eclampsia and normotensive women. This ratio yielded a sensitivity of 61.54%, specificity 87.84%, positive predictive value 64%, and negative predictive value of 86.67%. It was also observed that primigravida had more sensitivity (83.3%) and specificity (91.7%) in predicting pre-eclampsia compared to multigravida. The mean and median UCCR among pre-eclamptic women was significantly low (0.062 ± 0.076, 0.03) compared to normotensive women (0.15 ± 0.115, 0.12) with a p value of < 0.001. Spot UCCR is a good predictor of pre-eclampsia in primigravida women and can be considered as a routine screening test at 20-28weeks of gestation during regular antenatal visits.

Hypercalcemia in the setting of HTLV-1 infection and a normal PTHrP level

SummaryHuman T-cell lymphotropic virus-1 (HTLV-1) causes adult T-cell leukemia and lymphoma (ATLL) and is a rare but important cause of hypercalcemia. A 53-year-old male with HTLV-1-associated myelopathy presented with acute on chronic bilateral lower extremity weakness and numbness. Initial blood work revealed hypercalcemia with corrected calcium of 16.2 mg/dL (8.5–11.5) with normal levels of phosphorus and alkaline phosphatase. Workup for hypercalcemia revealed parathyroid hormone (PTH) of 14 pg/mL (10–65), 25 hydroxy vitamin D at 19.6 ng/mL (30–100), 1,25 dihydroxy vitamin D at 6.7 pg/mL (19.9–79.3), thyroid-stimulating hormone of 1.265 μIU/mL (0.5–5), undetectable PTH-related protein (PTHrP) and lactate dehydrogenase of 433 U/L (100–220). The urine calcium creatinine ratio was 0.388. Reverse transcriptase PCR was positive for HTLV-1 and negative for HTLV-2. Peripheral blood flow cytometry and lymph node biopsy confirmed ATLL. He received treatment with fluids, calcitonin and denosumab after which serum calcium levels fell (nadir: 7.7 mg/dL) and then normalized. Humoral hypercalcemia in this setting is mediated by receptor activator of nuclear factor-kappa B ligand (RANKL), PTHrP and other cytokines. PTHrP levels depend on levels of the TAX gene product, cell type and lymphocyte-specific factors. Thus, a low level, like in our patient, does not rule out HTLV-1 infection/ATLL as the cause of hypercalcemia. Hypercalcemia is known to be responsive to monoclonal antibodies against RANKL given the compound’s role in mediating hypercalcemia in these cases.Learning pointsHuman T-cell lymphotropic virus-1 infection and adult T-cell leukemia and lymphoma are associated with high rates of hypercalcemia and hypercalcemic crises.Hypercalcemia in these cases is mediated by osteoclastic bone resorption carried out by several agents including receptor activator of nuclear factor-kappa B ligand, parathyroid hormone-related protein (PTHrP), macrophage inflammatory protein 1 alpha, interleukins, etc. A normal PTHRrP does not rule out humoral hypercalcemia of malignancy in this setting, as indicated by this case.Hypercalcemia in such settings is highly responsive to monoclonal antibodies against RANKL given the role the ligand plays in resorptive hypercalcemia.

A CASE SERIES ON HYPERCALCEMIA

Hypercalcemia in adults arises from a myriad of underlying causes. Etiology of hypercalcemia varies from causes like Vitamin D toxicity to hyperparathyroidism, hyperthyroidism, chronic kidney disease, granulomatous diseases, and malignant diseases .Though not an uncommon metabolic problem, hypercalcemia can easily be missed due to the diverse clinical presentations. Primary hyperparathyroidism and malignancy are the most common causes, accounting for 90% of the cases. Clinical manifestation varies depending on the ionized calcium levels. Symptoms manifest when calcium levels exceed 12 mg/dl. We report four different cases that illustrate the need for a focused workup of hypercalcemia. Routine hypercalcemia workup includes serum Parathormone (PTH), Vitamin D, ionized calcium, phosphorus, magnesium, alkaline phosphatase levels, renal functions, and urinary calcium-creatinine ratio. Prognosis depends on the cause of hypercalcemia. The clinical diagnosis needs a high index of suspicion. Denitive management requires focused workup for etiological diagnosis and treatment of underlying cause. Treatment for hypercalcemia is required in all symptomatic patients or if the calcium level exceeds more than 15 mg/dL, even if asymptomatic. Immediate management includes restoring intravascular volume and promoting diuresis. Calcitonin, Bisphosphonates and steroids play a role in medical management. For patient's refractory to medical treatment, hemodialysis is required.

A cohort study on use of the spot urine calcium-creatinine ratio for prediction of antepartum preeclampsia among high-risk pregnant women in Delta State, Nigeria

Background/Aim: Preeclampsia is a multisystemic disorder, which significantly contributes to maternal and fetal morbidity and mortality, especially in developing countries where it accounts for about one-third of maternal mortality cases. Predicting its occurrence will reveal a sizeable population of pregnant women who will undoubtedly benefit from prevention. The ideal screening marker for the disease is still being investigated. The urine calcium-creatinine ratio (CCR) is an inexpensive, simple, and easily assayed biomarker. This study determined the accuracy of the spot urinary calcium-creatinine ratio in predicting the occurrence of preeclampsia.&#x0D; Methods: This was a prospective cohort study conducted in Delta State, which involved four healthcare facilities in Nigeria. A total of 138 pregnant women between 8 and 18 weeks gestation were recruited. Urine samples were obtained at 18 weeks to assay their CCR, and patients were followed up weekly for blood pressure measurement and dipstick urinalysis until delivery.&#x0D; Results: The mean spot urine CCR in this study was 0.225 (0.101). It was significantly lower in women who developed preeclampsia compared to normotensive women (P &lt; 0.001). Multiple logistics regression analysis showed that the association between urine CCR and occurrence of preeclampsia was statistically significant. At a receiver operating characteristic cutoff of ≤ 0.1065, CCR had a sensitivity of 75%, specificity of 91.3%, positive predictive value (PPV) of 35.3%, and negative predictive value (NPV) of 98.3%. The low PPV of 35.3% can be explained by the low prevalence of preeclampsia (5.78%) in the study population.&#x0D; Conclusion: In conclusion, the poor PPV of the urine CCR was due to the low prevalence of preeclampsia in the study. However, in considering all women at risk, urine CCR may be a good prognostic marker when the illness prevalence is substantial.

Abstract 135: A case of acquired Gitelman syndrome presenting as hypokalemic paralysis and AKI

Introduction: Gitelman syndrome is usually an inherited disorder, it is induced by defect in the thiazide sensitive Na –Cl co-transporter in distal tubules. Case reports on hypokalemia, AKI secondary to GS has been discussed in present case report.Clinical Case: A 18 year old female referred from department of General Medicine as a case of AKI having recurrent hypokalemia. She gave history of hypokalemic paralysis. There was no potential cause of dehydration such as diarrhoea, vomiting, nephrotoxic agent intake or contrast exposure. Family history was negative. During current hospitalization, she was normotensive with normal renal function test. Other electrolyte levels including calcium and routine laboratory parameters were determined to be normal. Kidney dimensions and echogenicity were determined to be normal without hydronephrosis in the urinary system as oer USG finding. Further workup for hypokalemia revealed urine potassium creatinine ratio (17 mmol/g), ABG (pH 7.44, bicarbonate 26.5 mmol/l), urine chloride (111.3 mmol/l) and urine calcium creatinine ratio (0.05 mmol/mmol) respectively with serum Mg (1.7 mg/dl) on lower range. Based on above findings, a diagnosis of Gitelman syndrome has been made. Autoimmune etiology were ruled out. These finding suggested that patient had AKI secondary to hypokalemia. She was started on oral potassium supplementation and magnesium supplementation.Conclusion: GS is a rare tubulopathy transmitted as an autosomal recessive trait. It is caused by mutation in thiazide sensitive Na Cl co-transporter coding gene, SLC12A3. Patients may be referred with hypokalemia, hypomagnesemia and metabolic alkalosis associated muscular weakness and cramping. By contrast, worsening hypokalemia and profound volume depletion as the predisposing factors for ischemic AKI appears to coexist.

Evaluation of Urinary Calcium, Creatinine and their Ratio in Preeclampsia: A Case-control Study

Introduction: Preeclampsia is a hypertensive disorder characterised by high blood pressure during pregnancy. It is the major cause of maternal and perinatal morbidity and mortality in females. Prediction of Pregnancy Induced Hypertension (PIH) can be done by using a valuable marker i.e. Urinary CalciumCreatinine ratio (UCa/Cr). Aim: To evaluate the urinary calcium, creatinine and UCa/Cr ratio in patients with preeclampsia and also to check the association of UCa/Cr ratio with the severity of the disease. Materials and Methods: The present case-control study was conducted in the Department of Biochemistry in collaboration with department of Obsteritics and Gynecology, Maharishi Markandeshwar University, Ambala, Haryana from January 2018 to January 2021. Total of 120 pregnant women with gestational age ≥20 weeks (60 normal and 60 preeclampsia) were evaluated for urinary calcium, urinary creatinine and UCa/ Cr ratio. For statistical analysis, Unpaired t-test and Chi-square test and was applied. Results: The mean age of control group was 27.51±5.05 years and for case group was 29.8±5.49 years. The level of urinary calcium and urinary creatinine was found to be significantly (p-value&lt;0.001) lower in case group (3.54 mg/dL and 42.90 mg/dL respectively) as compared to control group (8.22 mg/dL and 80.40 mg/dL respectively). The level of UCa/Cr ratio was also significantly (p-value &lt;0.001) lower in case group (0.08±0.04) than control group (0.11±0.04) (p&lt;0.001). Conclusion: UCa/Cr ratio was significantly decreased in preeclampsia compared to normal pregnancy. UCa/Cr ratio in spot urine can be useful in identifying pregnant women at risk for preeclampsia.

A PROSPECTIVE STUDY ON THE EFFECTIVENESS OF URINE CALCIUM CREATININE RATIO AND MICROALBUMINURIA IN PREGNANCY AS A PREDICTOR OF PREECLAMPSIA

Aim:To analyse the role of urinary calcium creatinine ratio and microalbuminuria in prediction of preeclampsia. Method:Aprospective study was conducted in 200 pregnant mothers.Urine samples for estimation of calcium, creatinine and microalbumin were done and these mothers were followed up to term for analysis of association with preeclampsia. Results :In this study 11.5% were diagnosed to have preeclampsia. Among 200 patients, 23 had elevated BP, proteinuria and HELLPsyndrome. Conclusion:This study demonstrates the strong association between urinary calcium creatinine ratio and microalbumin in prediction of preeclampsia.

Predicting adverse outcomes in hypertensive obstetric cases by using spot urine calcium: Creatinine ratio

Background: Hypertensive disorders complicate upto 5-10% of pregnancies, 3.9% is preeclampsia the leading cause of both direct maternal and perinatal mortality. Mostly preeclampsia is diagnosed only after pathological changes are already established. The study being carried out to investigate the significance of urinary calcium-creatinine ratio in predicting the outcomes with hypertensive disorder of pregnancy. Methods: All women between the gestational ages 20 -28 weeks were taken into the study, spot urine sample was taken to measure the urinary calcium-creatinine-ratio. Ratio less than or equal to 0.04 was considered test positive and those with ratio of >0.04 was considered test negative.Results: 218 normotensive, 17Gestational hypertension, and 21 Preeclampsia were recruited fir the study. Urinary creatinine excretion among gestational hypertension and preeclampsia is more than normotensive women. Calcium excretion is low in preeclampsia compared to normotensive women. CCR was positive 87.69% of preeclampsia and 40% in gestational hypertension. We found that CCR was a better predictor of preeclampsia than gestational hypertension, with sensitivity of 73.81%, specificity of 95.18%.More maternal complications such as abnormal Doppler studies and HELLP syndrome among preeclampsia, and lower birth weight were noted among women with preeclampsia. More number of abnormal APGAR at 1’ and 5’ were noted in preeclampsia group.Conclusion: Spot Urine calcium-creatinine ratio of ≤0.04 in asymptomatic pregnant women between 20-28 weeks of pregnancy is a good predictor for hypertensive disorders of pregnancy, especially preeclampsia. We can also conclude that there is increased maternal and fetal morbidity among women complicated with hypertension than normotensive women.