The Urinary System and Its Disorders
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss in Understanding Medical Terms, 2020
Since the urinary system eliminates such a variety of wastes, alterations in urinary function can quickly alter the composition of the blood. Along with the lungs, the kidneys perform a significant function in maintaining acid-base balance in the body, primarily by tubular reabsorption of filtered bicarbonate and excretion of hydrogen ions released by nonvolatile acids. Thus, the urinary system is involved in metabolic acidosis of several types. Renal tubularacidosis is hypokalemic (abnormally low serum potassium) in nature, while hypoaldosteronism can lead to metabolic acidosis, which is hyperkalemic. Starvation can lead to ketoacidosis, and kidney failure leads to lactic acidosis.
Endocrinology of aging
Philip E. Harris, Pierre-Marc G. Bouloux in Endocrinology in Clinical Practice, 2014
The decrease in serum renin, renin activity, and aldosterone in aging individuals can result in hypoal-dosteronism. The decline in secretion or action of renin and aldosterone is of particular importance when individuals have a type 4 renal tubular acidosis (RTA) or mild renal failure. Some older patients may have low-normal aldosterone values. The serum aldosterone concentrations and urinary aldosterone excretion should be checked in older hyponatremia patients to evaluate if primary aldosteronism is a cause of the hyponatremia. In addition to evaluating for hypoaldosteronism, the medications of elderly individuals should be reviewed. Medications such as thiazides and serotonin reuptake inhibitors are more likely to cause hyponatremia in the elderly than in other age groups.
Perioperative Care
Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams in Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Heparin should be used with caution in patients with increased risk of bleeding, uncontrolled hypertension or liver or kidney impairment. Patients with diabetes mellitus or chronic kidney disease could experience hypoaldosteronism leading to hyperkalaemia. Electrolytes should therefore be monitored carefully, especially in patients who have raised plasma potassium or in those who are taking potassium-sparing medications. In general, heparin should not be used in patients with chronic kidney disease stage 4–5 (creatinine clearance <20 mL/min), as they are unable to excrete the product. Similarly, caution should be used for patients who are on other antiplatelet medication and heparin concomitantly, as this could potentiate bleeding risk.
A patent review of aldosterone synthase inhibitors (2014-present)
Published in Expert Opinion on Therapeutic Patents, 2022
Jun Wu, Xiao Ding, Xuefei Tan
As a key component of the renin-angiotensin-aldosterone system (RAAS), mineralocorticoid aldosterone has been well recognized for its principal role in regulating fluid and electrolyte balance [1]. It promotes renal sodium (Na+) and water reabsorption, and induces potassium (K+) and hydrogen (H+) excretion in epithelial cells of the distal nephron [2]. Not surprisingly, dysregulation of aldosterone, either excess or deficiency, has been linked to the clinical conditions of various cardiovascular and metabolic diseases. ‘Hyperaldosteronism’ (excess aldosterone) contributes to arterial hypertension (AH), congestive heart failure, and chronic kidney disease (CKD) [3,4]. Meanwhile, aldosterone deficiency or ‘hypoaldosteronism’ results in hyponatremia, hyperkalemia, and acidosis [5,6].
Formulation, optimization, and nephrotoxicity evaluation of an antifungal in situ nasal gel loaded with voriconazole‒clove oil transferosomal nanoparticles
Published in Drug Delivery, 2021
Ahmed K. Kammoun, Alaa Khedr, Maha A. Hegazy, Ahmad J. Almalki, Khaled M. Hosny, Walaa A. Abualsunun, Samar S. A. Murshid, Rana B. Bakhaidar
There was an obvious reduction in the renal parameters in animal groups treated with either the drug suspension or the VRC-NT-loaded in situ gel compared with the control group. VRC contributed to a reduction in the glucose level in the test groups compared with the control group because VRC could have caused renal tubular damage and diminished the glucose tubular reabsorption process (Chris Rathbun & Hoffman, 2002). The VRC also contributed to the elevation of serum creatinine and urea levels. This could be ascribed to renal tubule damage and its negative effect on the glomerular filtration process of urea, leading to the accumulation of such parameters in plasma (Hosny & Alhakamy, 2020). Furthermore, VRC apparently caused hyperkalemia in treated animals; such an effect could be due to the ability of VRC itself to cause hypoaldosteronism. Similar findings were reported in the literature (Somani et al., 2000). Hypoproteinemia might be responsible for the decreased serum calcium levels in the test samples. The sodium levels were slightly varied.
An infant presenting with failure to thrive and hyperkalaemia owing to transient pseudohypoaldosteronism: case report
Published in Paediatrics and International Child Health, 2018
Marieke De Clerck, Johan Vande Walle, Evelyn Dhont, Joke Dehoorne, Werner Keenswijk
In high-income countries, the differential diagnosis of the infant presenting with failure to thrive is usually broad and includes feeding difficulties with/or inadequate intake, e.g. insufficient breast-milk, errors in preparation of infant formulae and food allergies. Relevant essential investigations include urinalysis, complete blood count, electrolytes, renal function and liver enzymes [1]. Hyponatraemia and especially hyperkalaemia are uncommon in this setting but can be associated with life-threatening events. In early infancy, unless there is clear evidence of gastrointestinal fluid losses or renal dysfunction, these electrolyte abnormalities usually point to adrenal failure and, more specifically, to congenital adrenal hyperplasia (CAH), often owing to 21-hydroxylase deficiency with concomitant hypoaldosteronism [2] and transient pseudohypoaldosteronism (TPHA). In 1983, Rodriguez-Soriano et al. [3] described TPHA in children with urinary tract anomalies (UTA). Since then, there have been a number of reports of TPHA, usually associated with UTA and/or urinary tract infections (UTI) [3,4]. A 3-month-old infant is described who presented with failure to thrive, hyponatraemia and hyperkalaemia owing to TPHA.