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Showing posts with the label Nephrology

Perioperative Kidney protection..Pharmacology agents

Diuretics (furosemide/mannitol) While use of diuretics may improve urine output in the setting of acute kidney injury, again there is no evidence to support that they confer any improvement in outcomes measured (including need for RRT and mortality) . Furthermore, use of furosemide has been shown to be not only ineffective but also detrimental, associated with higher postoperative serum creatinine levels in cardiac patients . Of note, mannitol is often added to the priming solution used in CPB surgery. Although initially shown to confer some preventive benefits in children undergoing CPB surgery, these results have not been reproduced in repeat studies, with a suggestion that mannitol is actually associated with increased tubular injury when given in combination with dopamine . Theophylline Theophylline, an adenosine antagonist, in theory is proposed to preserve renal blood flow by attenuating vasoconstriction of renal vessels . Several small studies...

Pipercillin-Tazobactam plus Vancomycin...Bad for the kidneys?

Two recently presented abstracts at the 2012 Society of Critical Care Medicine conference suggest that the combination of vancomycin and piperacillin-tazobactam may lead to acute kidney injury (AKI) in the critically ill. There may also be evidence to suggest that piperacillin-tazobactam alone increases the risk of AKI. Both abstracts retrospectively compared patients who received either vancomycin alone or the combination of vancomycin and piperacillin-tazobactam. In both studies, the rates of AKI were significantly lower in patients treated with vancomycin alone as compared to patients receiving both vancomycin and piperacillin-tazobactam. Bottom line: Although the current evidence does not support a change in our clinical practice, more prospective studies exploring this topic are necessary. Min, et al.  Acute Kidney Injury in Patients Recieving Concomitant Vancomycin and Piperacillin/Tazobactam . Critical Care Medicine. December 2011. 39(12); p 200 Hellwig, ...

Rebound Pain after Dialysis...Searching for NON Dialyzable Opioid

Today I was covering the acute pain service...i had a case of 81 y/o female patient with ESRD and Lymphoma...she was maintained on Duragesic patch 25mcg..we are consulted because she is suffering of severe chest and back pain during dialysis.."yes it is Rebound pain"..a well known phenomenon that occurs when opioids get dialyzed ...SO i thought How to manage..and what opioid that will stay in during dialysis... Here is what I found: The factors that determine whether or not a drug is filtered during dialysis are the molecular weight (MW) of the compound and its degree of protein binding, volume of distribution (VD), and solubility (WS) Molecules less likely to be removed by dialysis have low MW and WS, are highly protein bound, and have a high VD.   Using these criteria, one would anticipate that morphine , a drug of relatively low protein binding and moderate WS, would be removed by dialysis   Whereas methadone...

Contrast Induced Nephropathy..Who at risk?

Despite the absence of precise prevalence rates, overall trends and risk factors have been observed. Overall, the incidence of CIN is thought to be low in patients with normal renal function, but it can be much higher in patients with underlying renal disease. In the general population, the incidence of CIN is estimated to be 1% to 6%. Among patients with normal baseline renal function, the incidence of CIN is estimated to be < 2%. In chronic kidney disease (CKD), the incidence increases to 12% to 27%. In patients with both CKD and DM, the incidence of CIN may be as high as 50%. Patients with acute MI undergoing angioplasty are at higher risk of CIN than patients undergoing elective interventions. Incidence rates of 15% have been reported in patients undergoing cardiac catheterization.

Creatinine and Mortality

In an epidemiologic study of 19,982 adults admitted to an urban academic medical center, Chertow et al. reported that increases in SCr of 0.3 to 0.4 mg/dl were   significantly associated with in-hospital mortality (multivariable OR 1.7;   95% CI, 1.2 to 2.6).  These individuals experienced a roughly 70% increase in the risk of death compared with patients with   little or no change in SCr. Note that the significance of a change of 0.3 mg/dL depends on the baseline Cr.  For a given change in creatinine, the change in creatinine reflects a greater change in GFR at lower Cr levels compared with higher levels, i.e. early changes in Cr are more signficant. For example, an increase in Cr from 1 to 1.5 roughly correlates with a 33% drop in GFR.  An increase in Cr from 4 to 4.5 roughly correlates with a 5% drop in GFR.   The gross relationship is GFR ≈ 1/Cr . Chertow GM, Burdick E, Honour M, Bonventre JV, Bates DW. Acute kidney injury, mort...

Renal failure...LR better than NaCl

Traditionally balanced salt solutions  like LR were avoided in Renal failure patients  because of concerns regarding accumulation of potassium in renal failure.Keep in mind LR contains only 4 meq of potassium.... However, a study by O’Malley et al. demonstrated a 20% absolute risk increase (number needed to treat: 5) for hyperkalemia in patients undergoing renal transplantation who were administered saline rather than lactated Ringer solution. Moreover, there was a 30% incidence of metabolic acidosis, requiring treatment, in the saline group, versus 0% in the lactated Ringer group. Chloride is involved with regulation of renal vascular tone. Hansen demonstrated that potassium induced contraction of smooth muscle cells in the afferent arteriole is highly sensitive to chloride. Thus Chloride is a functional renal vasoconstrictor. Hyperchloremia has been shown to produce dose dependent renal vasoconstriction and a reduction in glomerular f...

Troponin in Renal disease

Up to 80% of patients with low glomerular filtration rates (GFR), and in the absence of acute coronary syndromes or congestive heart failure, have positive values for TnT, regardless of whether or not they receive dialysis treatment. On the other hand, one large study that included more than 700 patients found the prevalence of TnI to be only 0.4-6% depending on the cut-off value chosen . These results suggest that a positive TnT may represent a common and benign incidental finding in patients with impaired renal function, whereas a positive TnI occurs only in the setting of an acute coronary event. Tsutamoto et al. performed a very elegant study measuring the transcardiac TnT gradient by measuring levels in both the aortic root and coronary sinus . They classified 258 patients with congestive heart failure as having either normal or low GFR. Despite the finding of markedly elevated levels of TnT in the patients with low GFR compared to the patients with normal renal function, th...

Acidosis And Alkalosis .... SID

First of all Strong Ion Difference SID means SID = ([Na+] + [K+] + [Ca2+] + [Mg2+]) – ([Cl] + [other strong anions: A]) = 40–44 mEq If all other factors (PCO 2, albumin, and phosphate) are kept constant, an increase in SID will decrease hydrogen ion liberation from water (and increase hydroxyl ion liberation), causing alkalosis Decrease in SID increases hydrogen ion liberation, to maintain electrical neutrality, causing acidosis The chief determinant of SID is the relationship between the relative concentration of sodium, chloride and free water in ECF The normal ratio of sodium to chloride is approximately 1.4:1. Any process that reduces that ratio reduces SID and leads to acidosis (sodium loss, chloride gain, or free water gain). Any process that increases that ratio increases SID and leads to alkalosis (sodium gain, chloride loss, or free water gain) Second Acid–base disturbances are an importantnpart of clinical and laboratory investigation of perioperative and critical...

7 lethal effects of metabolic acidosis

The net effect of severe metabolic acidosis: Impaired cardiac contractility Decreased threshold for V-Fib Decreased Hepatic and Renal flow Increased pulmonary vascular  resistance Inability to respond to vasopressors Inhibition of coagulation factors and platelets vascular collapse

Kidneys failure...The Basics

Approximately 1 million nephrons are present in each kidney. Only after the GFR has decreased by 50% ('renal reserve') will there be an increase in plasma solutes such as urea and Cr. Chronic Kidney Disease defined as a decreased GFR of < 60mL/min/1.73m Kidney Failure defined as  GFR < 15mL/min/1.73m. The 2 leading causes of Chronic Renal Failure are DIABETES & HYPERTENSION The 5 year survival rate for patients undergoing chronic dialysis is 35%. The life expectancy of a 60 year old starting hemodialysis is 4 years vs 20 years for a healthy 60 year old. Patients with Chronic Kidney Disease generally don't manifest symptoms until the GFR < 30mL/min (Stage 4 & 5).

Perioperative Kidney Dysfunction and Protection

Perioperative acute renal failure is a common complication of major surgery and is associated with increased morbidity and mortality. Ischaemia- or toxin-mediated acute tubular necrosis is the primary cause of perioperative acute renal failure. The key non-pharmacological strategies are intravascular volume expansion, maintenance of renal blood flow and renal perfusion pressure, avoidance of nephrotoxic agents, careful glycaemic control, and the appropriate management of post-operative complications. At present, there is no firm evidence to suggest that the use of any specific pharmacological intervention is clinically beneficial. Dopamine infusion has not been shown to prevent acute renal failure, avert the need for renal replacement therapy, or reduce mortality, and should not be administered solely for renal protection. Contin Educ Anaesth Crit Care Pain (2008) 8 (5): 176-180