Session 2
What to order for a Kidney failure patient?
Labs: CMP (to check electrolytes, GFR, and trend creatine and differentiate acute or chronic kidney disease)
UA- check for hematuria, protein, nitrites, red blood cell casts, white blood cell casts
Albumin to creatine ratio
CBC- to check for anemia
Imaging: renal Ultrasound, non-contract CT of the abdomen
Session 3
What is AKI?
AKI is defined by a rise in the serum creatinine concentration or an abnormal urinalysis that has developed within hours to days. Consensus criteria for AKI include:
- an increase in serum creatinine by ≥0.3 mg/dL (27 micromol/L) relative to a known baseline value within 48 hours
- or an increase to ≥1.5 times the known or presumed baseline value within seven days
- or a decrease in urine volume to <3 mL/kg over six hours
Acute Kidney Injury results in retention of nitrogenous and other wastes products normally cleared by the kidneys.
Common causes of AKI are sepsis, major surgical procedures, heart and liver failure, and nephrotoxic medication.
AKI is divided into 3 categories prerenal azotemia, intrinsic renal parenchymal disease, and postrenal obstruction. Prerenal being the most common form. There is a rise in serum creatinine and BUN due to inadequate renal plasma flow. The most common clinical conditions are hypovolemia, decreased cardiac output, and medications.
Prolonged periods of prerenal azotemia may lead to ischemic injury, often termed acute tubular necrosis (ATN)
Sepsis-induced ATN is often associated with prerenal factors such as decreased renal perfusion and systemic hypotension. Among the critically ill, sepsis is the most common cause of ATN. The likelihood of renal tubule injury with sepsis is increased if there are concurrent adverse clinical characteristics, including older age, underlying renal or liver insufficiency, and additional factors. There are many factors that contribute to sepsis-induced ATN. Some factors are hypotension, direct renal vasoconstriction, and release of cytokines. Additionally even in settings with moderate volume depletion the risk of renal failure can increase in the presence of nephrotoxins.
Nephrotoxins are toxic agents or substances that inhibits, damages or destroys the cells and/or tissues of the kidneys. Examples of nephrotoxic drugs are Vancomycin, Aminoglycosides, heme pigments, cisplatin, radiocontrast media, pentamide, foscarnet, cidofovir, IV immunoglobulin, mannitol. These agents impede the kidney’s ability to get rid of excess urine, and wastes.
Anion Gap Metabolic Acidosis
Indicates that there is a fall in bicarb or an increase in acids. Causes include Ketoacidosis can occur as a complication of type I diabetes mellitus (diabetic ketoacidosis), but can occur due to other disorders, such as chronic alcoholism and undernutrition. In these conditions, excessive free fatty acid metabolism results in the production of ketoacids, acetoacetic acid, and beta-hydroxybutyrate.
Lactic acidosis results from excess formation and decreased metabolism of lactate, which occurs during states of anaerobic metabolism. It is the most common cause of metabolic acidosis in hospitalized patients. The most serious s form occurs during various states of shock, due to episodes of decreased liver perfusion. Lactic acidosis commonly occurs with tissue hypoperfusion that may be secondary to systemic hypotension
Kidney failure results in decreased acid excretion and increased bicarbonate excretion. Patients with severe renal failure may develop a high anion gap acidosis, resulting from the retention of both hydrogen ions and anions such as sulfate, phosphate, and urate
Toxins that result in acidic metabolites may trigger lactic acidosis. Rhabdomyolysis, a muscle-wasting disease, is a rare cause of metabolic acidosis.
the normal value for the serum anion gap is now approximately 3 to 10 mEq/L
COVID-19 is associated with AKI. Patients with suspected or confirmed COVID-19 may present with acute kidney injury (AKI) as part of their overall illness. In observational data from Wuhan, AKI has been reported in 25 to 29 percent of patients who were critically ill or deceased The incidence of AKI among patients who are less severely ill is unknown.
In patients with suspected or confirmed COVID-19 who develop AKI, an emphasis should be placed on optimization of volume status to exclude and treat prerenal (functional) AKI while avoiding hypervolemia, which may worsen the patient’s respiratory status. The evaluation for other AKI etiologies should be undertaken in a manner similar to other critically ill patients with AKI. As an example, manual urine sediment examination should be performed, if appropriate, since urine samples are not considered to be highly infectious. In some cases COVID-19 patients with AKI will require dialysis.
Differences in management of AKI among patients with COVID-19 infection may include limited use of intravenous fluids. Most patients with COVID-19 infection characterized by pneumonia have variable degree of oxygen requirements and/or airway control. Fluid resuscitation goals are understandably conservative as per various acute respiratory distress syndrome criteria. Thus, fluid resuscitation should be individualized and based on trackable objective measures
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