scholarly journals A Rare Case of Patiromer Induced Hypercalcemia

2021 ◽  
Vol 10 (16) ◽  
pp. 3756
Author(s):  
Swetha Rani Kanduri ◽  
Kathryn J. Suchow ◽  
Juan Carlos Q. Velez
Keyword(s):  
Serum Calcium ◽  
Serum Potassium ◽  
High Serum ◽  
Daily Routine ◽  
Acid Base Balance ◽  
Stage 4 ◽  
Ckd Stage ◽  
Base Balance ◽  
Baseline Creatinine ◽  
Renal Tubular

Patiromer is a calcium (Ca)-potassium (K) exchange resin approved for the treatment of hyperkalemia. Disorders of Ca or acid base balance were not reported in pre-approval clinical trials. We present a case of a patient with chronic kidney disease (CKD) with an unusual picture of hypercalcemia, metabolic alkalosis and hypokalemia upon intensification of patiromer dosing. A 56-year-old white man with CKD stage 4 (baseline creatinine 2.8 mg/dL) due to type 1 diabetes mellitus, proteinuria (1.5 g/g) and persistently high serum potassium 5.9 mEq/L attributed to type 4 renal tubular acidosis was evaluated in clinic. Due to high risk of CKD progression, patiromer 8.4 g daily, followed by 16.8 g daily was prescribed to enable renin angiotensin aldosterone system (RAAS) inhibitor. After 5 months of being on patiromer 16.8 g daily, routine laboratory tests revealed serum potassium 2.5 mEq/L, serum calcium 12.8 mg/dL and carbon dioxide 34 mEq/L. Patiromer was discontinued and thorough investigation held was negative for other causes of hypercalcemia. Five days after patiromer discontinuation, serum calcium returned to normal. The role of secondary hyperparathyroidism in this case remains unclear. We, therefore recommend cautious vigilance of patients receiving patiromer and undergoing dose escalation.

scholarly journals Exhausted Capacity of Bicarbonate Buffer in Renal Failure Diagnosed Using Point of Care Analyzer

Diagnostics ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 226
Author(s):  
Tomasz Gołębiowski ◽  
Mariusz Kusztal ◽  
Andrzej Konieczny ◽  
Magdalena Kuriata-Kordek ◽  
Ada Gawryś ◽  
...  
Keyword(s):  
Point Of Care ◽  
Venous Blood ◽  
Cross Sectional Study ◽  
Acid Base Balance ◽  
Cross Sectional ◽  
Bicarbonate Buffer ◽  
Ckd Stage ◽  
Base Balance ◽  
Group A ◽  
Group B

Background: Metabolic acidosis in patients with chronic kidney disease (CKD) is a common complication. A bicarbonate concentration in venous blood (V-HCO3−) is a key index for diagnosis and treatment initiation. The aim of our study is to evaluate usability of acid–base balance parameters of in blood taken simultaneously from peripheral artery and the vein. Methods: A total of 49 patients (median age 66 years [interquartile range IQR 45–75]), with CKD stage G4 or G5 were enrolled in this cross-sectional study. All patients were qualified for arteriovenous fistula creation in pre-dialysis period. The samples were taken during surgery, directly after dissection, and evaluated in a point of care testing analyzer. The arteriovenous difference in bicarbonate levels (Δ-HCO3−) was calculated. According to glomerular filtration rate (eGFR) the group was divided into Group A eGFR ≥ 10 mL/min/1.73 m2) and Group B eGFR < 10 mL/min/1.73 m2). Results: In Group A Δ-HCO3− was significantly higher compared to Group B. No such differences were observed in the case of V-HCO3−. Δ-HCO3− positively correlated with eGFR. The discriminative power of Δ-HCO3− for predicting eGFR < 10 mL/min/1.73 m2 was 0.72 (95% confidence interval [CI] = 0.551–0.88; p = 0.01) which provided 67% sensitivity and 75% specificity. The best cut-off was 0.5 mmol/L. Conclusions: The Δ-HCO3− lower than 0.5 mmol/L may be used as predictor of exhaust buffer capacity. The value of this tool should be tested in larger population.

Histopathological and biochemical evaluations of the kidney inbroiler chickens under acute heat stress conditions.

2017 ◽  
Author(s):  
S.C. Huang ◽  
Y.F. Fu ◽  
Y.F. Lan ◽  
M.U. Rehman ◽  
Z.X. Tong
Keyword(s):  
Heat Stress ◽  
Broiler Chickens ◽  
Serum Markers ◽  
Acid Base Balance ◽  
Tubular Necrosis ◽  
Acute Heat Stress ◽  
Tubular Lumen ◽  
Base Balance ◽  
Histopathological Images ◽  
Renal Tubular

The purpose of the present study was to investigate the correlation between acute heat stress and relevant histopathology and biochemical parameters of kidney function. A total of 80 healthy Arbor Acer (AA) broiler chickens were randomly divided into two groups: CT (Control Temperature; 22±1°C) group and HT (High Temperature; 38±1°C) group. Histopathological images revealed alteration in kidney (renal tubular lumen dilation with tubular necrosis, especially after 10h of heat stress) of broiler chickens in HT group leading to disturbance of acid base balance. Blood urea nitrogen (BUN) and creatinine (CREA) as serum markers of renal dysfunction were elevated significantly (p less than 0.05) after 5h, and especially, after 10h of heat stress (p less than 0.01) as compared with CT group. These results indicated that the evaluation of morphological and functional parameters in kidney is required, in order to monitor broiler chickens exposed to heat stress.

scholarly journals Roles of Renal Proximal Tubule Transport in Acid/Base Balance and Blood Pressure Regulation

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Motonobu Nakamura ◽  
Ayumi Shirai ◽  
Osamu Yamazaki ◽  
Nobuhiko Satoh ◽  
Masashi Suzuki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ang Ii ◽  
Acid Base Balance ◽  
Acid Base ◽  
Blood Pressure Homeostasis ◽  
Base Balance ◽  
Proximal Renal Tubular Acidosis ◽  
Renal Tubular ◽  
Regulation Of Blood Pressure

Sodium-coupled bicarbonate absorption from renal proximal tubules (PTs) plays a pivotal role in the maintenance of systemic acid/base balance. Indeed, mutations in the Na+-HCO3-cotransporter NBCe1, which mediates a majority of bicarbonate exit from PTs, cause severe proximal renal tubular acidosis associated with ocular and other extrarenal abnormalities. Sodium transport in PTs also plays an important role in the regulation of blood pressure. For example, PT transport stimulation by insulin may be involved in the pathogenesis of hypertension associated with insulin resistance. Type 1 angiotensin (Ang) II receptors in PT are critical for blood pressure homeostasis. Paradoxically, the effects of Ang II on PT transport are known to be biphasic. Unlike in other species, however, Ang II is recently shown to dose-dependently stimulate human PT transport via nitric oxide/cGMP/ERK pathway, which may represent a novel therapeutic target in human hypertension. In this paper, we will review the physiological and pathophysiological roles of PT transport.

THE PROXIMAL RENAL TUBULAR TRANSPORT OF α-KETOGLUTARIC ACID

1963 ◽  
Vol 41 (1) ◽  
pp. 1099-1104
Author(s):  
P. Vishwakarma
Keyword(s):  
Proximal Tubule ◽  
Physicochemical Characteristics ◽  
Tubular Secretion ◽  
Acid Base Balance ◽  
Concentration Gradients ◽  
Base Balance ◽  
Active Transfer ◽  
Renal Tubular Transport ◽  
Renal Tubular ◽  
Active Reabsorption

The transport of α-ketoglutaric acid along the length of the renal tubule was studied by the stop-flow method in the dog during infusion of sodium α-ketoglutarate. No deliberate attempts to change the acid–base balance were made. Under these conditions this acid was found to be excreted by a combined process of glomerular filtration and tubular reabsorption. This reabsorption was confined only to the proximal tubule. No tubular secretion was seen in any part of the nephron. The concentration gradients between the luminal urine, cell water and the plasma were measured. It was seen that the gradients between the lumen and the cell and between the lumen and the plasma were against the direction of the transport. The gradient between the plasma and the cell was favorable to the uptake of the acid by the cell. Upon consideration of these gradients, the spontaneous pH changes and the physicochemical characteristics of the molecule, the hypothesis was forwarded that an active reabsorption of α-ketoglutarate must occur in the proximal tubule from the lumen into the cell. The possibility of active transfer of this acid from the blood into the cell was also suggested.

Renal Medicine

2019 ◽  
Author(s):  
William White
Keyword(s):  
Vitamin D ◽  
Clinical Medicine ◽  
Collecting Duct ◽  
Objective Structured Clinical Examination ◽  
Junior Doctors ◽  
Acid Base Balance ◽  
Electrolyte Homeostasis ◽  
Base Balance ◽  
Stimulation Of Erythropoiesis ◽  
Renal Tubular

The kidney causes problems for medical students and junior doctors alike— the convoluted journey from plasma to urine, the conundrum of what is reabsorbed and excreted where, and the tangled web of the glomerulonephritides are traditionally learnt, rather than actually understood. As in all clinical medicine, a good place to start is with the fundamen­tals of the organ in question. Passage from plasma to urine follows the pathway: ● Blood ● Glomerulus ● Tubules ● Collecting duct ● Ureter ● Bladder ● Urethra. The primary functions of the kidney are: ● Removal of toxins ● Electrolyte homeostasis ● Maintenance of acid– base balance ● Activation of vitamin D ● Stimulation of erythropoiesis ● Maintenance of blood volume. The challenge then is to implement these basics by being sensitive to deviations from normal physiology: recognizing the accumulation of any potential toxins (hyperkalaemia, uraemia, and acidosis) or the lack of any synthetic products (hypocalcaemia and anaemia), suggesting triggers for such deviations, and pinpointing the specific parts of the anatomy that may be malfunctioning in some way so as to cause impairment. Despite its bad reputation, the kidney reveals more about itself than any other organ and, in theory, should be the easiest to monitor. It achieves this through its raison d’être: urine. Its presence, absence, con­tents, smell, and colour offer a running commentary on the activity of the renal tract at any given point in time— it is the internal, intangible work­ings of specialized cells made physical, measurable, and dippable. So, far from being those much- feared Objective Structured Clinical Examination (OSCE) stations, the dipstick and the catheter are our friends. Or they should be, for it is our ability to harness the information that they pro­vide, allied to the series of numbers on the oft- requested ‘U&Es’ (urea and electrolytes), against a background of wide- ranging symptoms that will make us sensitive to the running of the kidney. This— not just our ability to regurgitate the three types of renal tubular acidosis— is what is at stake in this chapter.

Clinic and diagnosis of metabolic nephropathies in children

1986 ◽  
Vol 67 (5) ◽  
pp. 358-360
Author(s):  
S. V. Maltsev ◽  
V. M. Davydova ◽  
E. I. Zemlyakova
Keyword(s):  
Uric Acid ◽  
Acid Content ◽  
Acid Metabolism ◽  
Calcium Phosphates ◽  
Xanthurenic Acid ◽  
Acid Base Balance ◽  
Residual Nitrogen ◽  
Daily Urine ◽  
Base Balance ◽  
Renal Tubular

We examined 70 patients with metabolic nephropathy (51 with oxaluria predominance, 19 with uric acid metabolism disorders). Distribution of patients into groups was carried out according to the results of multistage research, including analysis of pedigree; repeated biochemical studies, clinical and radiological comparisons. Endogenous creatinine clearance, residual nitrogen level, urea in blood, acid-base balance were determined to characterize the functional state of the kidneys. Renal tubular function was assessed by urinary excretion of calcium, phosphates, amino acids, titratable acids, Zimnitsky's test. To detect metabolic disorders we studied uric acid content in blood and urine, oxalic acid and xanthurenic acid content in daily urine.

Renal Tubular Acidosis in Children Treated With Trimethoprim-Sulfamethoxazole During Therapy for Acute Lymphoid Leukemia

PEDIATRICS ◽  
1992 ◽  
Vol 89 (6) ◽  
pp. 1072-1074
Author(s):  
Jerome Linus Murphy
Keyword(s):  
Renal Tubular Acidosis ◽  
Elevated Serum ◽  
Growth Failure ◽  
Serum Bicarbonate ◽  
Acid Base Balance ◽  
Urine Ph ◽  
Lymphoid Leukemia ◽  
Acute Lymphoid Leukemia ◽  
Base Balance ◽  
Renal Tubular

The antibiotics trimethoprim (TMP) and sulfamethoxazole (SMZ), when used in combination, can cause metabolic acidosis, renal bicarbonate wasting, and growth failure. Retrospective review of repeated random serum chemistries from 10 children receiving TMP-SMZ and maintenance chemotherapy for acute lymphoid leukemia revealed low serum bicarbonate (P = .0002) and elevated serum chloride (P &lt; .0005) concentrations. These values normalized after all medications were discontinued. Prospective study of 8 children receiving TMP-SMZ and chemotherapy for acute lymphoid leukemia revealed lower serum bicarbonate concentrations and higher urine pH following a dose of TMP-SMZ than paired values obtained more than 3 days after a dose. Four children (50%) met serum bicarbonate and urinary pH criteria for the diagnosis of renal tubular acidosis soon after a dose of TMP-SMZ. The occurrence of TMP-SMZ-induced renal tubular acidosis has implications for the acid-base balance of children receiving TMP-SMZ on a long-term basis.

Renal medicine

2018 ◽  
pp. 649-698
Author(s):  
Drew Provan
Keyword(s):  
Kidney Diseases ◽  
Stone Disease ◽  
Rational Approach ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Acid Base Balance ◽  
Renal Bone Disease ◽  
Base Balance ◽  
Diagnosis And Classification ◽  
Renal Tubular

This chapter reviews the investigations required for the diagnosis and classification of acute and chronic kidney diseases. Detailed guidance is provided on the choice of methods to measure or estimate the glomerular filtration rate and to quantify albuminuria/proteinuria. It offers a rational approach to the choice of blood and urine tests in the investigation of patients presenting with haematuria, proteinuria, renal tubular dysfunction, and disorders of acid–base balance. It reviews the pertinent radiological investigations used alongside specialist urine and immunology tests to aid diagnosis. There is a detailed review of the rational investigation of patients with recurrent kidney stone disease. Guidance is provided on laboratory investigation of suspected renal bone disease and on the role of renal biopsy in the investigation of kidney disease.

Two classic papers in acid-base physiology: contributions of R. F. Pitts, R. S. Alexander, and W. D. Lotspeich

2004 ◽  
Vol 287 (5) ◽  
pp. F864-F865 ◽  
Author(s):  
Gerhard Giebisch
Keyword(s):  
Acid Base Balance ◽  
Acid Base ◽  
Historical Significance ◽  
Base Balance ◽  
Renal Tubular ◽  
Classic Papers

This essay looks at the historical significance of two APS classic papers that are freely available online: Pitts RF and Alexander RS. The nature of the renal tubular mechanism for acidifying the urine. Am J Physiol 144: 239—254, 1945 ( http://ajplegacy.physiology.org/cgi/reprint/144/2/239 ). Pitts RF and Lotspeich WD. Bicarbonate and the renal regulation of acid base balance. Am J Physiol 147: 138—154, 1946 ( http://ajplegacy.physiology.org/cgi/reprint/147/1/138 ).

THE PROXIMAL RENAL TUBULAR TRANSPORT OF α-KETOGLUTARIC ACID

1963 ◽  
Vol 41 (5) ◽  
pp. 1099-1104 ◽  
Author(s):  
P. Vishwakarma
Keyword(s):  
Proximal Tubule ◽  
Physicochemical Characteristics ◽  
Tubular Secretion ◽  
Acid Base Balance ◽  
Concentration Gradients ◽  
Base Balance ◽  
Active Transfer ◽  
Renal Tubular Transport ◽  
Renal Tubular ◽  
Active Reabsorption

The transport of α-ketoglutaric acid along the length of the renal tubule was studied by the stop-flow method in the dog during infusion of sodium α-ketoglutarate. No deliberate attempts to change the acid–base balance were made. Under these conditions this acid was found to be excreted by a combined process of glomerular filtration and tubular reabsorption. This reabsorption was confined only to the proximal tubule. No tubular secretion was seen in any part of the nephron. The concentration gradients between the luminal urine, cell water and the plasma were measured. It was seen that the gradients between the lumen and the cell and between the lumen and the plasma were against the direction of the transport. The gradient between the plasma and the cell was favorable to the uptake of the acid by the cell. Upon consideration of these gradients, the spontaneous pH changes and the physicochemical characteristics of the molecule, the hypothesis was forwarded that an active reabsorption of α-ketoglutarate must occur in the proximal tubule from the lumen into the cell. The possibility of active transfer of this acid from the blood into the cell was also suggested.

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