Acute kidney failure resident survival guide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Acute Renal Failure is an abrupt reduction in kidney function defined as at-least one of the following: 1. an absolute increase in the serum levels of creatinine of 26.4 μmol/L(0.3mg/dl) or more; 2. a percentage increase in the serum levels of creatinine of more than 50%(1.5 fold increase from baseline); or 3. a reduction in volume of urine output(oliguria <0.5 ml/kg hourly for >6 hours. Acute renal failure is increasingly common, particularly in elderly population, hospital inpatients, and critically ill patients and it carries a high mortality. The most common cause of in-hospital acute renal failure in acute tubular necrosis resulting from multiple nephrotoxic insults such as sepsis, hypotension, and use of nephrotoxic drugs or radio-contrast media. Patients at risk include elderly people, diabetics, patients with hypertension or vascular disease, and those pre-existing renal impairment. To aid the diagnosis and management, it is important to find out the underlying cause, whether its pre-renal, renal or post renal. Initial workup should be carried out as soon as the patient is encountered and any life threatening situation should be treated promptly.

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• Life threatening cause 1
• Life threatening cause 2
• Life threatening cause 3

Pre Renal Causes

• Hypovolaemia

* Haemorrhage

* Volume depletion(for example vomiting, diarrhea, burns, inappropriate diuresis)

• Renal Hypoperfusion

* Non-steroidal anti-inflammatory drugs/selective cyclo-oxygenase 2 inhibitors

* Angiotension converting enzyme inhibitors/angiotension receptor antagonist

* Abdominal aortic aneurysm

* Renal artery stenosis/occlusion

* Hepatorenal syndrome

• Hypotension

* Cardiogenic shock

* Distributive shock(for example sepsis, anaphylaxis)

• Oedematous States

* Cardiac failure

* hepatic cirrhosis

* Nephrotic syndrome

Intrinsic Renal Causes

• Glomerular disease

* Inflammatory- post-infectious glomerulonephritis, cryoglobulinaemia, Henoch-Schonlein purpura, systemic lupus erythematosus, antineutrophil cytoplasmic antibody associated glomerulonephritis, anti-glomerular basement membrane disease

* Thrombotic- disseminated intravascular coagulation, thrombotic microangiopathy

• Interstitial Nephritis

* Drug Induced- Non-steriodal anti-inflammatory drugs, antibiotics

* Infiltrative- Lymphoma

* Granulomatous- Sarcoidosis, Tuberculosis

* Infection related- post-infective, Pyelonephritis

• Tubular Injury

* Ischemia- prolonged renal hypoperfusion

* Toxins- drugs(such as aminoglycosides), radiocontrast media, pigments(such as myoglobin), heavy metals(such as cisplatinum)

* Metabolic- hypercalcemia, immunoglobin light chains

* Crystals- urate, oxalate

• Vascular

* Vasculitis(usually associated with antineutrophil cytoplasmic antibody)

* Cryoglobulinaemia

* Polyarteritis nodosa

* Thrombotic microangiopathy

* Cholesterol emboli

* Renal artery thrombosis/renal vein thrombosis

Post Renal Causes

• Intrinsic

* Intra-luminal- stone, blood clot, papillary necrosis

* Intra-mural- urethral stricture, prostatic hypertrophy or malignancy, bladder tumor, radiation fibrosis

• Extrinsic

* pelvic malignancy

* retroperitoneal fibrosis

Diagnosis

Shown below is an algorithm summarizing an step by step approach to diagnosis the cause of Acute Renal Failure to aid in the management.

Patient presenting features ❑ Oliguria (sudden or gradual) ❑ Anuria ❑ Edema ❑ Hypotension ❑ Hematuria ❑ loin pain ❑ renal colic ❑ bone pain ❑ fever

Medical History and Risk Factors ❑ inquire about previous similar episodes ❑ co-morbidities ❑ Diabetes-long standing poorly controlled diabetes can precipitate ARF ❑ Hypertension ❑ Heart Failure ❑ Vascular disease(such as Renal Artery stenosis ❑ Inquire about drug history ❑ ACE inhibitors- can precipitate ARF in Renal artery stenosis ❑ NSAIDs-associated with interstitial kidney disease ❑ Penicillins-associated with renal papillary necrosis ❑ inquire about recent hospitalization-rule out Acute Tubular Necrosis ❑ Inquire about recent trauma/surgery-rule out sepsis-look for fever and hypotension/rule out hemorrhage and hypovolemia ❑ Age factor-elderly people-rule out Benign Prostate hypertrophy/prostate cancer ❑ elderly patient with bone pain-Myeloma? ❑ history of kidney stones<br ❑ Associated symptoms ❑ Nasal stuffiness/epistaxis-suggest Wagener's Granulomatosis? ❑ recent sore throat-streptococcal Glomerulonephritis ❑ Social history-Alcohol use/tobacco use/drug abuse ❑ history of autoimmune disorders- Systemic Lupus Erythromatosus, Good Pasture syndrome

Initial work-up ❑ Basic Blood ❑ full blood count with differentials ❑ blood glucose ❑ urea and electrolytes ❑ coagulation screen ❑ inflammatory markers ❑ urea/electrolytes ❑ liver function test ❑ calcium and phosphate ❑ blood culture if infection suspected ❑ Arterial blood gases or venous bicarbonate ❑ Urine analysis ❑ Urine microscopy/urine sediment/culture ❑ Renal ultrasound ❑ chest radiograph ❑ Electrocardiogram ❑ renal biopsy may be indicated if intrinsic cause is suspected

Draw a conclusion ❑ Treat any life threatening features first—shock, respiratory failure, hyperkalaemia ❑ Is this acute or chronic renal impairment? ❑ A full drug history (current, recent, and alternative medication) is vital ❑ Is there a pre‐renal cause? What is the patient's current fluid status? ❑ Could this be obstruction? ❑ Is intrinsic renal disease probable—what does urine analysis show?

Treatment

Definitive Management depends upon the underlying cause; however, initial approach is directed to treat any life threatening feature attempting to halt or reverse the decline the renal function, and if unsuccessful providing support by renal replacement anticipating renal recovery . Hyperkalemia, pulmonary edema and severe acidosis require immediate attention.

1.HYPERKALEMIA TREATMEMT-Severe hyperkalemia is a medical emergency and should be immediately treated with infusion of calcium. Treatment with calcium is a temporising measure “buying time” while measures are started to reduce the serum potassium through increasing cellular uptake. Overall these measures will bring the potassium back to normal;however, still body will be in excess. If pure pre-renal failure, measures can be taken to excrete the potassium through kidney by giving resins. Ultimately, if hyperkalemia is refractory to all above measures, hemodialysis ca be started.

Serum potassium>6.5 is a medical emergency

Immediate action

Reduction in plasma potassium concentration

Removal of potassium from the body

Calcium gluconate or carbonate

If pure pre-renal failure, renal excretion will serve to return the whole body levels to normal

to stabilize the myocardium and prevent cardiac arrythmias

Ion exhange resins calcium polystrene or sodium polystrene

Hemodialysis for refractory hyperkalemia

Insulin with glucpse

beta-2 agonist

Sodium bicarbonate

2.TREATING PULMONARY EDEMA-Pulmonary oedema is often the result of excessive fluid resuscitation, and can be anticipated in many patients—especially those with known cardiac dysfunction, the elderly, and those who appear volume replete at the outset—and hopefully avoided by more judicious intravenous fluid therapy. If respiratory failure, intubate the patient and start mechanical ventilation.While these measures are being undertaken, pharmacological treatment to offload the decompensated heart can be started. If these measures fail, hemodialysis or hemofiltration can be used.

PULMONARY EDEMA

Respiratory failure

Pharmacological treatment

I/V opioids(diamorphine)

I/V infusion of glyceryl nitrate

provoke diuresis with large doses of diuretics such as furesemide

Supplemental oxygen OR intubate and mechanically ventilate

3.TREATING ACIDOSIS-Severe metabolic acidosis (blood pH <7.2) often accompanies ARF and arises through a variety of mechanisms, related both to reduced renal function and the underlying cause of the patient's illness. Systemic acidosis impairs cardiac contractility, induces bradycardia, produces vasodilatation, and augments hyperkalaemia, among other effects. Reversing acidosis through administration of an alkaline solution—sodium bicarbonate—would seem to be sensible, but there is very little evidence to show that it provides benefit. Isotonic (1.26%) solutions may have a role as fluid replacement therapy in stable patients with a moderate to severe acidosis and a requirement for fluid replacement, in whom dialysis is not imminent. Haemodialysis or haemofiltration will usually be required to treat severe acidosis in oligoanuric patients.

4.OTHER GENERAL MEASURES

Do's

• Normal Saline is preferred fluid for resuscitation.
• Treat acute renal failure keeping in mind the cause behind it.
• Start Dialysis when needed.
• Correction of coagulopathy if needed with DDAVP and cryoprecipitate.
• DVT prophylaxis if needed.
• Avoid pressure ulcers.

Don'ts

• Avoid fluid overload.
• Dont use dopamine to increase renal perfusion.
• cautious use of diuretics if oliguria persists.
• Don't use nephrotoxic drugs (NSAIDs, ACE-I, Aminoglycosides)
• Avoid use of contrast media.

References

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KEY POINTS ❑ Fluid Balance-normal saline preferred but avoid fluid overload ❑ Relief of Obstruction-Bladder outflow obstruction if suspected should be relieved by passage of urethral catheter ❑ Uremic Platelet Dysfunction-Renal replacement therapy may improve but DDAVP and cryoprecipitate may be required ❑ Carbohydrate and protein requirement should be tailored individually and ideally delivered by enteral route ❑ Practice good infectious control ❑ Care of pressure areas ❑ DVT prophylaxis if prolonged immobility