ACUTE RENAL FAILURE

BY

DR UCHENNA ONYENUCHE

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BINGHAM UNIVERSITY

• Acute renal failure (ARF) is a clinical syndrome in which a sudden deterioration in renal function results in the inability of the kidneys to maintain fluid and electrolyte homeostasis.
• It is a potentially reversible condition.
• It has recently been recoined as Acute Kidney Injury(AKI).

• Acute kidney injury was proposed to redefine the entire spectrum of acute renal dysfunction, encompassing early and mild forms all the way to severe forms requiring renal replacement therapy.
• This was done by RIFLE classification.

• Risk
• Injury
• Failure
• Loss
• End stage kidney disease

This relied on changes in the serum creatinine or glomerular filtration rates and/or urine output.

Causes

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The causes of acute failure are pre-renal, intrinsic renal, or Post-renal .

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Pre-renal

• Prerenal AKI is functional response of structurally normal kidneys to hypoperfusion, resulting usually from any process that decreases renal blood flow to the glomeruli e.g
• Dehydration   
• Hemorrhage   
• Sepsis    
• Cardiac failure
• Burns

Intrinsic Renal

• Intrinsic renal AKI involves structural damage to the renal parenchyma.
• It may results from failure to reverse any cause of prerenal AKI.
• Intrinsic renal AKI may also be caused by direct toxicity to the tubules from medications and other nephrotoxins, also from interstitial and glomerular diseases.

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• Acute Glomerulonephritis
•  Lupus erythematosus  
• Hemolytic-uremic syndrome
• Renal vein thrombosis
• Rhabdomyolysis
• Tumor lysis syndrome
• Acute pyelonephritis

Post-Renal

• Postrenal AKI is caused by obstruction to urinary flow.
• Posterior urethral valves   
• Ureteropelvic junction obstruction   
• Ureterovesicular junction obstruction      
• Urolithiasis  
• Neurogenic bladder

Features

• Features of precipitating cause e.g dehydration
• Oliguria/anuria
• Edema
• Convulsion and coma
• hypertension, vomiting and lethargy

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• Aminoglyoside nephrotoxicity and contrast nephropathy are more likely to have ARF with normal urine output.

Investigations

• Serum Electrolyte, Urea and Creatinine
• Full blood count.
• Laboratory abnormalities depend on the cause and may include anemia, metabolic acidosis, elevated serum concentrations of blood urea nitrogen, creatinine, potassium, and phosphate.

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• Chest radiography may reveal cardiomegaly and pulmonary congestion (fluid overload).
• Renal ultrasonography may reveal hydronephrosis and/or hydroureter, which are suggestive of urinary tract obstruction.

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Treatment

• First decide the type; pre-renal, intrinsic-renal or post-renal.

Pre-renal

• Intravascular volume should be expanded by intravenous administration of isotonic saline, 20 mL/kg over 30 min.
• Severe hypovolemia may require additional fluid boluses.
• After volume resuscitation, hypovolemic patients generally void within 2 hr; failure to do so points toward the presence of intrinsic ARF.

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• Diuretic therapy should be commenced after the adequacy of the circulating blood volume has been established.
• Mannitol (0.5 g/kg) and furosemide (2–4 mg/kg) may be administered to enhance urine output.

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Intrinsic-renal

• If there is no response to a diuretic challenge, diuretics should be discontinued and fluid restriction becomes essential.
• Patients should be limited to 400 mL/m²/24 hr (insensible losses) plus an amount of fluid equal to the urine output for that day.
• Restrict salt intake.

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• Extrarenal fluid losses should be replaced, ml for ml, with appropriate fluids.
• Fluid input and output, body weight, and serum chemistries should be monitored on a daily basis.
• Correct electrolyte derangements.
• Other conservative management should take care of hyperkaelemia, acidosis, hypocalcemia, hyponatremia, hypertension, seizures, anaemia.

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Post-renal

• Urethral, suprapubic or nephrostomy drainage may be required.
• There may be marked diuresis with relief of the obstruction and the fluid balance must be strictly monitored.

• Indications for dialysis in ARF include the following:

-Pulmonary edema refractory to diuretic therapy.       

-Persistent hyperkalemia. 

-Severe metabolic acidosis unresponsive to medical management.   

-Neurologic symptoms (altered mental status, seizures).

   -Calcium/phosphorus imbalance, with hypocalcemic tetany

Prognosis

• Prognosis of ARF depends on the underlying condition, but is generally good in childhood.

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CHRONIC RENAL FAILURE

• Chronic renal failure, also called Chronic kidney disease (CKD) is defined as either renal injury (proteinuria) and/or a glomerular filtration rate <60 mL/min/1.73 m² for at least 3 months.
• Often accompanied by other biochemical abnormalities.

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Etiology

• The underlying cause correlates closely with the age of the patient at the time when the CKD is first detected.
• In children younger than 5 yr is most commonly a result of congenital abnormalities such as renal hypoplasia, dysplasia, and/or obstructive uropathy.
• Additional causes polycystic kidney disease, renal vein thrombosis, and hemolytic uremic syndrome.

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• After 5 yr of age, acquired diseases like glomerulonephritis and inherited disorders, Alport syndrome) predominate.
• Other causes of CRF include hemolytic uremic syndrome, chronic pyelonephritis, congenital single kidney, hypertension.

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Features/Pathophysiology

• Accumulation of nitrogenous waste products and Acidosis : Decrease in glomerular filtration rate, impaired bicarbonate reabsorption, decreased net acid excretion.
• Solute diuresis:   Tubular damage , urinary concentrating defect .
• Hyperkalemia: Decrease in glomerular filtration rate, metabolic acidosis hyporeninemic hypoaldosteronism .

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• Renal osteodystrophy: Impaired renal production of 1, 25 dihydroxycholecalciferol ,hyperphosphatemia,   hypocalcemia, secondary hyperparathyroidism.
• Growth retardation: Inadequate caloric intake ,renal osteodystrophy  metabolic acidosis, anemia.

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• Anemia: It is a normochromic, normocytic anaemia. It may be due to decreased erythropoietin production, hemolysis in uremic patients, chronic gastrointestinal bleeding.
• Bleeding tendency :Defective platelet function.  

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• Neurologic symptoms: Headache, drowsiness, seizures, peripheral neuropathy, uremic factor, hypertension.
• Infection :Defective granulocyte function , impaired cellular immune functions ,indwelling dialysis catheters.
• Hypertension : Volume overload, excessive renin production.

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• Pericarditis/cardiomyopathy Uremic factor, hypertension, fluid overload.

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Investigations

• Laboratory findings include elevations in blood urea nitrogen and serum creatinine.
• Laboratory findings may also reveal hyperkalemia, hyponatremia, acidosis, hypocalcemia, hyperphosphatemia, and an elevation in uric acid.
• A complete blood cell count usually shows a normochromic, normocytic anemia.

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• In children with CKD caused by glomerulonephritis, the urinalysis shows hematuria and proteinuria.
• Renal Ultrasound- Shrunken kidneys.

Treatment

• Management is conservative.
• Oliguric or anuric patents should receive fluid equal to their insensitive loss plus the previous 24hrs urine volume.
• Diuretics may be used to treat edema and oliguria.
• If serum bicarbonate is less than 15mmol/L sodium bicarbonate may be given.

• Give antihypertensives to control blood pressure.
• Give phosphate binders e.g calcium carbonate are used to treat hyperphosphatemia.
• Recombinant human erythropoietin to treat anaemia.
• Avoid nephrotoxic drugs e.g gentamicin

• Vitamin D(1, 25 dihydroxy cholecalciferol) administration is the cornerstone of therapy for renal osteodystrophy .
• Children with CKD should receive all standard immunizations according to the schedule used for healthy children.
• Treat dyselectrolytaemia.
• Adequate nutrition.

End-Stage Renal Disease

• ESRD is the state in which a patient's renal dysfunction has progressed to the point at which homeostasis and survival can no longer be sustained with native kidney function and maximal medical management.
• At this point, renal replacement therapy (dialysis or renal transplantation) becomes necessary.

DIALYSIS

• It is the process of removing   excess water, solutes, and toxins from the blood in people whose kidneys can no longer perform these functions naturally.
• Should be a temporary measure while the possibility of transplantation is being pursued, as a permanent measure in those for whom a transplant is not possible.

• It is a form or renal replacement therapy.
• Dialysis works on the principles of the diffusion of solutes and ultrafiltration of fluid across a semi-permeable membrane, it removes wastes and excess water from the blood in different ways.
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• The two main types of dialysis are: hemodialysis and peritoneal dialysis.
• Hemodialysis removes wastes and water by circulating blood outside the body through an external filter, called a dialyzer, that contains a semipermeable membrane.

• In peritoneal dialysis, wastes and water are removed from the blood inside the body using the peritoneum as a natural semipermeable membrane.