Complications of Antibiotic Therapy
Stephen M. Cohn, Matthew O. Dolich in Complications in Surgery and Trauma, 2014
Before the advent of the lipid formulations of amphotericin B, the deoxycholate form of the drug was commonly referred to as amphoterrible B, because of the acute systemic reaction it caused, including fever and rigors, as well as dose-dependent renal failure. There is an expected reversible azotemia, with creatinine rising up to 2–3 g/dL. Treatment should continue despite this azotemia. The most important side effect of amphotericin B is dose-related nephrotoxicity, with the destruction of the renal tubules. This toxicity may be attenuated by the use of liposomal or lipid emulsion preparations. These effects are very much attenuated with the lipid preparations of the drug.45 Although rare, anaphylaxis has been associated with both amphotericin–deoxycholate and liposomal amphotericin B.46
Surgical management of adult and pediatric renovascular hypertension
Sachinder Singh Hans, Alexander D Shepard, Mitchell R Weaver, Paul G Bove, Graham W Long in Endovascular and Open Vascular Reconstruction, 2017
The outcomes of carefully selected patients with renal arteriosclerotic disease undergoing open surgical treatment for their RVH result in 25% cure, 55% improvement, and 20% failure rates, with a reported mortality rate of 3%.1−8 Renal function is improved in approximately 15%, unchanged in 75%, and worsened in 10%. The latter is often a reflection of pre-existing renal dysfunction, with chronic azotemia portending a poor response to any intervention. Acute complications, occurring <3% of the time, include thrombotic occlusions due to a distal renal artery flap or technical failures of a bypass graft associated with anastomotic narrowing. Late complications of both endarterectomy and bypass procedures are usually due to neointimal narrowing causing recurrent RVH in 5% of cases.
Kanamycin
M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson in Kucers’ The Use of Antibiotics, 2017
Similar to other aminoglycosides, kanamycin may cause renal damage. Kanamycin is not as nephrotoxic as neomycin, but it is thought to be more toxic than streptomycin, which is possibly the least nephrotoxic aminoglycoside (Appel and Neu, 1977). The incidence of nephrotoxicity in the treatment of TB varies from 4.5% to 9% (de Jager and van Altena, 2002; Peloquin et al., 2004). Patients developing nephrotoxicity in one study were more likely to have received prolonged kanamycin courses and larger cumulative doses (de Jager and van Altena, 2002). Kanamycin accumulates in renal cortical tissue (Buss et al., 1984) and can cause changes in the proximal tubules that range from cloudy swelling to acute necrosis. Mild renal toxicity with the appearance of casts, red and white cells, and protein in the urine is relatively common. Increasing azotemia is infrequent, except perhaps in older patients. Oliguric renal failure with features of acute tubular necrosis may occasionally develop. Recovery from these more severe nephrotoxic effects is usually slow and may be only partial (Appel and Neu, 1977; Bennett et al., 1977). Early recognition of kanamycin nephrotoxicity is also important because it may predispose patients to ototoxicity (Finegold, 1959; 1966), although more recent studies could not find a link between these two toxicities (Peloquin et al., 2004; Smith et al., 1979).
Leptospirosis in the elderly: the role of age as a predictor of poor outcomes in hospitalized patients
Published in Pathogens and Global Health, 2019
Elizabeth De Francesco Daher, Douglas de Sousa Soares, Gabriela Studart Galdino, Ênio Simas Macedo, Pedro Eduardo Andrade de Carvalho Gomes, Roberto da Justa Pires Neto, Geraldo Bezerra da Silva Junior
AKI was defined according to the ‘Kidney Diseases Improving Global Outcomes’ (KDIGO) criteria, which is the currently most accepted definition and classification for AKI [8]. The occurrence of metabolic acidosis was evidenced when pH <7.35 and serum bicarbonate <20 mEq/L, and severe metabolic acidosis when pH <7.10. Tachypnea was defined as a respiratory rate higher than 25 per minute. Oliguria was defined as urine output <0.5 ml/kg/day after 24 h of effective hydration. Hypotension was defined as mean arterial blood pressure (MAP) <60 mmHg. Therapy with vasoactive drugs was initiated when MAP remained lower than 60 mmHg despite the use of endovenous fluids. Azotemia was defined as serum urea >120 mg/dL, which represents an elevation three times higher than the normal range. Hyponatremia was defined as serum sodium <135 mEq/L.
Hyperkalemia in chronic peritoneal dialysis patients
Published in Renal Failure, 2022
Andrew B. Elliott, Karim M. M. Soliman, Michael E. Ullian
We found that serum samples with higher [K+]s also contained higher creatinine concentrations and urea nitrogen concentrations. Similar to our findings were those from Liu et al., who observed a positive correlation between azotemia (creatinine and urea nitrogen levels) and [K+]s [17]. It is possible that noncompliance with PD therapy, which would be reflected by more azotemia, caused hyperkalemia. It is also possible that larger muscle mass or greater protein intake contributed to hyperkalemia. It has been demonstrated that skeletal muscle content of potassium is greater in PD patients than in control patients with normal renal function [21]. A carefully performed metabolic study in 8 chronic PD patients demonstrated that increasing daily dietary protein intake from 0.98 to 1.44 g/kg resulted in positive nitrogen balance and positive potassium balance [22]. We did not find that hyperkalemia-only patients were younger than hypokalemia-only patients, with youth a putative marker of larger muscle mass.
Terrible TR: A Marker or Maker of Cardiac Dysfunction?
Published in Structural Heart, 2019
Stephen H. Little, Paul A. Grayburn
Although multiple forms of cardiac dysfunction will negatively impact forward flow and cardiac output, TR is somewhat unique in its additional impact on venous congestion of the visceral organs. Renal dysfunction in particular is often simplistically associated with pre-renal azotemia secondary to reduced perfusion volume. However, organ prefusion (and performance) depends not only on the delivery of blood, but also on the trans-renal pressure gradient. Several years ago, Mullens and colleagues4 reported that venous congestion was the most important hemodynamic factor for worsening renal function in patients with advanced decompensated heart failure. While the recognition is not new that renal (and hepatic) venous congestion contribute to excess morbidity and mortality, it is now appropriate to more fully consider the role of significant TR in this cascade of additional organ dysfunction.