Drug-Induced Electrolyte Disorders

1983 ◽  
Vol 17 (3) ◽  
pp. 175-185 ◽  
Author(s):  
Amin A. Nanji

A wide variety of pharmacologic agents have been implicated in a number of electrolyte disorders. The present review focuses on abnormalities of sodium, potassium, calcium, magnesium, and phosphate. Several mechanisms are involved in the pathogenesis of these disorders. These involve stimulation and modulation of other hormones (e.g., antidiuretic hormone, renin-angiotensin system, parathyroid hormone), damage to renal tubules, and, in some cases, a combination of factors. Recognition of these abnormalities is important because their presence may be life threatening or may aggravate the side effects of the drug itself.

Fluid and electrolyte disorders are very common in nephrology practice. They may develop due to several disorders related directly with kidney disease, or with other conditions or drugs, etc., altering fluid and electrolyte physiology. Fluid and electrolyte disorders may usually present as an incidental finding in a blood test with mild or no symptoms, but may also present as a severe, life-threatening entity. Fluid and electrolyte disorders may present as single, isolated derangement of one electrolyte or as mixed problems. The prevention or prompt recognition and appropriate management of fluid and electrolyte disorders protect redundant morbidities and mortalities in many patients. This chapter covers disorders of sodium, potassium, calcium, phosphate and magnesium, and acid-base. It also discusses the clinical use of diuretics, which have dual effect on fluid-electrolyte disorders as aetiologic or therapeutic agents.


1983 ◽  
Vol 245 (2) ◽  
pp. F131-F141 ◽  
Author(s):  
D. W. Ploth

Our understanding of the physiology of the renin-angiotensin system has advanced remarkably in the last decade as a result of the development of several pharmacologic agents that effectively block components of this humoral cascade. The use of these antagonists has also advanced our understanding of the contribution of the renin-angiotensin system to the development and maintenance of two-kidney, one-clip renal vascular hypertension. These antagonists have contributed greatly to the characterization of the systemic hemodynamic changes that occur in this model and, particularly, to the delineation of the behavior of the nonclipped kidney, a previously normal kidney that is subjected acutely to an environment of elevated systemic blood pressure and the input of a variety of other extrinsic influences. This kidney not only allows the blood pressure to increase and persist at elevated levels but appears to actively participate in the development and propagation of the hypertension. Although a variety of mechanisms impinge on the function of the nonclipped kidney in this model, the goal of this review is to analyze the behavior of this kidney and how its functional state is perturbed, primarily by the influence of angiotensin, which is believed to be delivered to it by the systemic circulation.


2011 ◽  
Vol 16 (1) ◽  
pp. 130-135 ◽  
Author(s):  
Fumihiko Koiwa ◽  
Daisuke Komukai ◽  
Makoto Hirose ◽  
Ashio Yoshimura ◽  
Ryoichi Ando ◽  
...  

2021 ◽  
Vol 22 (4) ◽  
pp. 1705
Author(s):  
Silvia D’Amico ◽  
Patrizia Tempora ◽  
Valeria Lucarini ◽  
Ombretta Melaiu ◽  
Stefania Gaspari ◽  
...  

Patients with coronavirus disease 2019 (COVID-19) have a wide variety of clinical outcomes ranging from asymptomatic to severe respiratory syndrome that can progress to life-threatening lung lesions. The identification of prognostic factors can help to improve the risk stratification of patients by promptly defining for each the most effective therapy to resolve the disease. The etiological agent causing COVID-19 is a new coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that enters cells via the ACE2 receptor. SARS-CoV-2 infection causes a reduction in ACE2 levels, leading to an imbalance in the renin-angiotensin system (RAS), and consequently, in blood pressure and systemic vascular resistance. ERAP1 and ERAP2 are two RAS regulators and key components of MHC class I antigen processing. Their polymorphisms have been associated with autoimmune and inflammatory conditions, hypertension, and cancer. Based on their involvement in the RAS, we believe that the dysfunctional status of ERAP1 and ERAP2 enzymes may exacerbate the effect of SARS-CoV-2 infection, aggravating the symptomatology and clinical outcome of the disease. In this review, we discuss this hypothesis.


2019 ◽  
Vol 317 (2) ◽  
pp. F333-F342 ◽  
Author(s):  
Vanesa Palau ◽  
Julio Pascual ◽  
Maria José Soler ◽  
Marta Riera

It is known that the renin-angiotensin system plays a major role in the pathophysiology of cardiovascular disease and renal injury. Within the renin-angiotensin system, angiotensin-converting enzyme 2 (ACE2) cleaves ANG II to generate ANG(1–7) peptide, which counteracts the adverse effects of ANG II accumulation. ACE2 can undergo cleavage or shedding to release the catalytically active ectodomain into the circulation by a disintegrin and metalloprotease (ADAM)17, also known as TNF-α-converting enzyme. ADAM17 is involved in many pathological processes such as cancer, inflammatory diseases, neurological diseases, cardiovascular diseases, atherosclerosis, diabetes, and hypertension. Clinical and experimental studies have shown that ADAM17 is involved in chronic kidney disease (CKD) with a proinflammatory and profibrotic role, suggesting that it could be an important mediator of CKD progression. ADAM17 inhibition attenuates fibrosis and inflammation, suggesting that its inhibition may be a possible new valuable therapeutic tool in fibrotic kidney disease treatment. In addition, in renal disease, some experimental studies have demonstrated that ADAM17 is differently expressed in the kidney. Thus, ADAM17 is highly expressed in distal renal tubules and increased in the whole kidney in diabetic models. In this article, we will review the role of ADAM17 under physiological and pathological conditions. We will mainly focus on the importance of ADAM17 in the context of CKD.


2020 ◽  
Vol 48 (9) ◽  
pp. 030006052095949
Author(s):  
Jae Won Kim ◽  
Goo Kim ◽  
Tae Woo Kim ◽  
Woong Han ◽  
Mo Se Kim ◽  
...  

Vasopressin local infiltration is useful in gynecological surgery because it can reduce hemorrhage. Depending on the activities of the sympathetic system and the renin–angiotensin system, reactions to vasopressin may differ and predicting its systemic effects is difficult. Because life-threatening complications can occur, infiltration with vasopressin should be administered with caution. A 42-year-old female patient was diagnosed with uterine leiomyomas. During a robot-assisted laparoscopic myomectomy, 50 U of vasopressin, which is ten-times the recommended dose, was accidentally infiltrated. Subsequently, bradycardia with a heart rate of 25 bpm occurred, which recovered within 3 minutes. Peripheral perfusion indices and the diameter of the radial and brachial arteries also decreased markedly and recovered within 1 hour. The surgery was concluded without additional events. The patient was discharged 2 days later with no abnormal findings. Because vasopressin infiltration can cause life-threatening complications, it is necessary to determine the extent of patient reactions to vasopressin using measures such as the peripheral perfusion index or radial and brachial artery diameters. These measures may also help to predict the occurrence of complications.


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