Renal compensation

Angina is a common problem in older adults When an older adult requires an antianginal drug, the dosage maybe reduced to compensate for impaired renal function or heart disease. Older patients are at increased risk for postural hypotension. Blood pressure and ability to ambulate should be monitored closely. 

Metabolic alkalosis is characterized by an increased arterial pH, a primary increase in the HCOf concentration, and a compensatory increase in the PaC02. Patients will always hypoventilate to compensate for metabolic alkalosis—even if it results in profound hypoxemia. For a metabolic alkalosis to persist there must concurrently be a process that elevates serum HC03 concentration (gastric or renal loss of acids) and another that impairs renal HC03 excretion (hypovolemia, hypokalemia, or mineralocorticoid excess). The etiologies of metabolic alkalosis are listed in Table 25-5. 

The goals of therapy in patients with chronic respiratory acidosis are to maintain oxygenation and to improve alveolar ventilation if possible. Because of the presence of renal compensation it is usually not necessary to treat the pH, even in patients with severe hypercapnia. Although the specific treatment varies with the underlying disease, excessive oxygen and sedatives should be avoided, as they can worsen C02 retention. 

If symptoms do not improve, the patient should be evaluated for persistent infection. There are many reasons for poor patient outcome with intraabdominal infection improper antimicrobial selection is only one. The patient maybe immunocompromised, which decreases the likelihood of successful outcome with any regimen. It is impossible for antimicrobials to compensate for a nonfunctioning immune system. There may be surgical reasons for poor patient outcome. Failure to identify all intraabdominal foci of infection or leaks from a GI anastomosis may cause continued intraabdominal infection. Even when intraabdominal infection is controlled, accompanying organ system failure, most often renal or respiratory, may lead to patient demise. 

Renal function impairment- In patients with impaired renal function (Ccr less than 60 mL/min), adjust the dose of cefepime to compensate for the slower rate of renal elimination. The recommended initial dose should be the same as in patients with normal renal function. 

Renal function Impairment- Ceftazidime is excreted by the kidneys, almost exclusively by glomerular filtration. In patients with impaired renal function (glomerular filtration rate (GFR) less than 50 mL/min), reduce dosage to compensate for slower excretion. In patients with suspected renal insufficiency, give an initial loading dose of 1 g. Estimate GFR to determine the appropriate maintenance dose. 

Renal function impairment- In adult patients with impaired renal function, adjust the dose of didanosine to compensate for the slower rate of elimination. 

Excess HCOf is managed to some extent by respiratory compensation (hypoventilation) but mainly by an increase in renal HCOf excretion. 

Management has three important caveats. Firstly, it is mandatory that the causative lesion be reliably identified and, if possible, corrected. Here it should be remembered that a suboptimal intake of this vitamin is frequently seen in those who have diets deficient in vegetables and particularly fresh leafy products found in salads. Secondly, once treatment is initiated, there may be precipitous falls in serum potassium as ineffective haematopoiesis suddenly corrects and so removes the substantial delivery of the intracellular cation to the circulation renal compensation requires slightly longer to adapt and in that interval cardiac arrhythmia and death can occur. Eor this reason patients either need to have plasma electrolytes monitored initially or arbitrary oral potassium replacement supplied. Thirdly, there may be a transient increase in haemoglobin, which then reaches a plateau, and this is the consequence of exhausting available iron stores so that monitoring is necessary or supplementation with simple ferrous salts provided. 

A related issue is the patient s ability to metabolize and eliminate drugs adequately. For example, lithium is excreted entirely by the kidneys, and if a patient suffers from significantly impaired renal function, high, potentially toxic levels could develop on standard doses. Although the dose could be adjusted to compensate for the decrease in drug clearance, it might be more appropriate to choose another mood stabilizer such as valproate or carbamazepine, because they are primarily metabolized through the liver. 

S) Increased risk of renal toxicity Blockade of normal compensation for cardiodepressant effects (S)... 

Sodium phosphate is available as a nonprescription liquid formulation and by prescription as a tablet formulation. When taking these agents, it is very important that patients maintain adequate hydration by taking increased oral liquids to compensate for fecal fluid loss. Sodium phosphate frequently causes hyperphosphatemia, hypocalcemia, hypernatremia, and hypokalemia. Although these electrolyte abnormalities are clinically insignificant in most patients, they may lead to cardiac arrhythmias or acute renal failure due to tubular deposition of calcium phosphate (nephrocalcinosis). Sodium phosphate preparations should not be used in patients who are frail or elderly, have renal insufficiency, have significant cardiac disease, or are unable to maintain adequate hydration during bowel preparation. 

Most ACE inhibitors are eliminated primarily via the kidney. However, fosinoprilat is excreted about equally in the bile and urine (148). Biliary excretion can compensate for compromised renal function, and thus blood levels of fosinoprilat remain relatively constant in patients with varying degrees of renal impairment (150). 

The limitations of the Jaffe method for creatinine determination are discussed under Assessment of Renal Injury by Serum Chemistry . Exogenous creatinine clearance compensates for the insensitivity of the method as well as the interference by endogenous chromagens by artificially increasing the plasma creatinine concentration (Finco 1997). 

Urea and creatinine elevations in plasma are in general not sensitive enough to detect low-level alterations (less than 75 % loss) in functional nephron mass, due to the contribution of renal secretion and/or reabsorption to their overall excretion, (which can compensate for their decreased filtration), to wide variations in baseline levels of some analytes, and to inherent imprecision in the assays used (Finn and Porter 1998 Price 2002 Starr et al. 2002 Shemesh et al. 1985). In particular, urea will underestimate GFR (due to extensive tubular reabsorption with decreased GFR) (Baum et al. 1975 Kaplan and Kohn 1992 Newman and Price 1999). Creatinine tends to overestimate GFR because it is secreted by the tubule in many species and secretion increases with reduced GFR (Shemesh et al. 1985 Andreev et al. 1999 Newman and Price 1999 Starr et al. 2002). In addition, creatinine synthesis is regulated by feedback inhibition which limits the degree of elevation than can occur in plasma with renal injury (Watson et al. 2002). 

In compensated cirrhosis, sodium retention can occur in the absence of vasodilatation and effective hypovolaemia. Sinusoidal portal hypertension can reduce renal blood flow even in the absence of haemodynamic changes in the systemic circulation, suggesting the existence of a hepatorenal reflex. Portal hypertension increases the hydrostatic pressure within the hepatic sinusoids and favours transudation of fluid into the peritoneal cavity. 

Metabolic acidosis involves a build-up of hydrogen ions in the blood, thus lowering blood pH. Under normal physiological conditions, the kidneys excrete excess hydrogen ions, and release more bicarbonate ions into the bloodstream to buffer the excess acid. However, in renal failure, or in diabetic ketoacidosis, this mechanism either fails, or is unable to compensate to an adequate extent. Hence, metabolic acidosis is usually treated with sodium bicarbonate, either intravenously (1.26% or 8.4% i.v. solution) or orally (typically 1 g three times a day). Sodium bicarbonate 1.26% intravenous solution is isotonic with plasma (and with sodium chloride 0.9%), so may be given in large volumes (1-2 L) by peripheral venous catheter to correct metabolic acidosis and provide fluid replacement at the same time. Sodium bicarbonate 8.4% may only be given by central venous catheter. 

Fortunately, the kidney has a remarkable ability to compensate for the loss of renal functional mass. Within a short time after unilateral nephrectomy, the remaining kidney hypertrophies such that overall renal function appears normal by standard clinical tests. Compensation becomes a problem when evaluating the effects of nephrotoxicants specifically, changes in kidney function may not be detected until the ability of the kidney to compensate is exceeded. Then, within a short period of time, an animal might develop life-threatening renal failure. 

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