Acute renal failure

Acute Renal Failure (Acute Kidney Injury)

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Acute Renal Failure ,Acute tubular Necrosis (Definition) Causes. Clinical presentations. Complications and Treatment. Preventions.
Objectives
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Acute Renal Failure (ARF)

ARF; also referred to as acute kidney injury (AKI) describes a sudden and usually reversible loss of renal function, which develops over days or weeks and is usually accompanied by a reduction in urine volume. Azotaemia: retention of urea and other nitrogen compounds in blood Uraemia : synonymous with azotaemia, also means uraemic syndrome, i.e., the clinical manifestation of renal failure
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Classifications of Renal Failure

Acute versus chronic Pre-renal, renal, post-renal Anuric, oliguric, polyuric
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Acute Versus Chronic

Acute Sudden onset Rapid reduction in urine output Usually reversible Tubular cell death and regeneration Chronic Progressive Not reversible Nephron loss 75% of function can be lost before its noticeable
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Acute Renal Failure
Pre-renal = 55% Renal parenchymal (Intrinsic)= 40% Post-renal = 5-15%
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Causes of ARF

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Clinical assessment

There may be marked hypotension and signs of poor peripheral perfusion, such as delayed capillary return. It may occur without hypotension like in NSAIDs, ACEI. Not always the cause of reduced blood flow is clear like in concealed blood loss can occur into the gastrointestinal tract, following trauma or in to into the pregnant uterus.
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Clinical assessment

In sepsis there is systemic circulatory vasodilation hence relative underfilling of the arterial tree even after fluid resuscitated. The combination of sepsis with nephrotoxins such as NSAIDs is a common cause of ARF.
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Patients with AKI may report symptoms such as anorexia, fatigue, nausea and vomiting, and pruritus, as well as a decline in urine output or dark-colored urine. Furthermore, if the patient has become volume overloaded, shortness of breath and dyspnea on exertion may be noted.
Clinical Manifestations
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On physical examination, findings such as asterixis, myoclonus, or a pericardial rub may be evident. If volume overload is present, peripheral edema, pulmonary crackles, and jugular venous distention may be found. It is also not unusual for a patient to be entirely asymptomatic, with advanced AKI discovered only by laboratory testing.
Clinical Manifestations
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Establish and correct the underlying cause of the ARF. If hypovolaemia is present, restore blood volume as rapidly as possible (with blood, plasma or isotonic saline (0.9%), depending on what has been lost).
Management
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Management

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Prognosis

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Established acute renal failure

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ATN may result from Ischaemia or Nephrotoxicity, caused by chemical or bacterial toxins, or a combination of these factors. Drugs which are toxic to renal tubular cells include the aminoglycoside antibiotics, such as gentamicin, the cytotoxic agent cisplatin, and the antifungal drug amphotericin B. Dead tubular cells may shed into the tubular lumen, leading to tubular obstruction
Acute tubular necrosis (ATN)
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During recovery, depending on the severity of the renal damage and the rate of recovery, there is often a diuretic phase in which urine output increases rapidly and remains excessive for several days before returning to normal. This is due in part to temporary loss of the medullary concentration gradient, and which depends on continued delivery of filtrate to the ascending limb of the loop of Henle and active tubular transport.
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Urine findings in Prenal azotemia vs. Acute Renal Failure

>1.018
<1.012
Urine osmolality
> 300 - 500
< 300 - 400

< 20 meq/l

> 40 meq/l

> 40

< 20

< 1
>2
Fractional excretion Na (U/P Na/ U/P creat)x100
<1
>2
Response to fluid challenge
++
?
Urine sediment
normal
hyaline cast brown granular casts, cellular debris
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Expansion of extracellular fluid volume. Hyperkalemia is a frequent complication of ARF; Coexistent metabolic acidosis may exacerbate hyperkalemia by promoting potassium efflux from cells. Hyperkalemia may be particularly severe, even at the time of diagnosis, in patients with rhabdomyolysis, hemolysis, and tumor lysis syndrome. Metabolic acidosis, often with an increased anion gap. Acidosis can be particularly severe when endogenous production of hydrogen ions is increased by other mechanisms (e.g., diabetic or fasting ketoacidosis; lactic acidosis complicating generalized tissue hypoperfusion, liver disease, or sepsis; metabolism of ethylene glycol or methanol).
Complications
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4. Hyperphosphatemia is an almost invariable complication of ARF. Severe hyperphosphatemia may develop in highly catabolic patients or following rhabdomyolysis, hemolysis, or tissue ischemia. Metastatic deposition of calcium phosphate can lead to hypocalcemia, 5. Anemia develops rapidly in ARF and is usually multifactorial in origin. Contributing factors include impaired erythropoiesis, hemolysis, bleeding, hemodilution, and reduced red cell survival time. 6. Prolongation of the bleeding time is also common. Common contributors to the bleeding diathesis include mild thrombocytopenia, platelet dysfunction, and/or clotting factor abnormalities (e.g., factor VIII dysfunction).
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7.Infection is a common and serious complication of ARF. 8.Cardiopulmonary complications of ARF include arrhythmias, pericarditis and pericardial effusion, and pulmonary edema. 9.Vigorous diuresis can occur during the recovery phase of ARF.
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Urea and creatinine. Electrolytes. Full blood count Clotting screen. Urinalysis. Renal ultrasound Others; Albumin, Chest X-ray, Serology and ECG.
Investigations
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In the absence of dialysis, the most common causes of death are Hyperkalaemia and Pulmonary oedema, followed by Infection and uraemia itself.
Management
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Therapy

Management Issue
Reversal of Renal Insult
Restore systemic hemodynamics and renal perfusion through volume resuscitation and use of vasopressors
Ischemic ATN
Eliminate nephrotoxic agents
Nephrotoxic ATN
Consider toxin-specific measures: e.g., forced alkaline diuresis for rhabdomyolysis, allopurinol/rasburicase for tumor lysis syndrome
Management of Ischemic and Nephrotoxic Acute Renal Failure
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Management of Ischemic and Nephrotoxic Acute Renal Failure
Therapy
Management Issue
Prevention and Treatment of Complications
Salt and water restriction
Intravascular volume overload
Diuretics
Ultrafiltration
Restriction of enteral free water intake
Hyponatremia
Avoidance of hypotonic intravenous solutions, including dextrose-containing solutions
Sodium bicarbonate (maintain serum bicarbonate >15 mmol/L or arterial pH >7.2)
Metabolic acidosis
Administration of other bases, e.g., THAM
Dialysis
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Hyperkalemia & EKG

K > 5.5 -6Tall, peaked T’sWide QRSProlong PRDiminished PProlonged QTQRS-T merge – sine wave *


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Therapy

Management Issue
Restriction of dietary K+ intake

Hyperkalemia

Eliminate K+ supplements and K+-sparing diuretics
Loop diuretics to promote K+ excretion
Potassium binding ion-exchange resins (e.g., sodium polystyrene sulfonate or Kayexelate)
Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote intracellular mobilization
Inhaled β-agonist therapy to promote intracellular mobilization Calcium gluconate or calcium chloride (1 g) to stabilize the myocardium
Dialysis
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Therapy

Management Issue
Calcium carbonate or gluconate (if symptomatic)
Hypocalcemia

Hypermagnesemia

Allopurinol, forced alkaline diuresis, rasburicase
Protein and calorie intake to avoid net negative nitrogen balance
Nutrition
To prevent complications of acute renal failure
Dialysis
Avoid other nephrotoxins: ACE inhibitors/ARBs, aminoglycosides, NSAIDs, radiocontrast unless absolutely necessary and no alternative
Choice of agents
Adjust doses and frequency of administration for degree of renal impairment
Drug dosing
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Marked volume overload. Severe metabolic acidosis. Hyperkalemia refractory to medical therapy. Pericarditis. Asterixis, Encephalopathy +Peripheral neuropathy. PEM. Anorexia, vomiting + nausea after exclusion of other causes. blood urea levels of >100 mg/dL
Absolute indications for dialysis include:
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In uncomplicated ARF mortality is low even when renal replacement therapy is required. In ARF associated with serious infection and multiple organ failure, mortality is 50-70%. Outcome is usually determined by the severity of the underlying disorder and other complications, rather than by renal failure itself.
Prognosis
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