Dr.Nahid Osman Ahmed 1

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2 ILOS By the end of the lecture you should be able to Identify : Functions of the kidney and nephrons Signs and symptoms of AKI Risk factors to AKI Treatment alternatives 2

3 Acute kidney injury (AKI), previously known as acute renal failure (ARF), is characterized clinically by an abrupt decrease in renal function over a period of hours to days, resulting in the accumulation of nitrogenous waste products (azotemia) and the inability to maintain and regulate fluid, electrolyte, and acid base balance. 3

4 Introduction Structure and Function of the kidney Primary unit of the kidney is the nephron 1 million nephrons per kidney Composed of a glomerulus and a tubule Kidneys receive 20% of cardiac output 4

5 Renal blood flow 5

6 Multiple function of the kidney 6

7 Pathophysiology of Kidney failure The production and elimination of urine requires three basic physiologic events: 1.Blood flow to the glomeruli 2.The formation and processing of ultra filtrate by the glomeruli and tubular cells 3.Urine excretion through the ureters, bladder and urethra 7

8 The clinical course of AKI has three distinct phases: 1-Oliguric Phase: a progressive decrease in urine production after kidney injury 2- Diuretic Phase: initial repair of the kidney insult with resultant diuresis of accumulated uremic toxins, waste products, and fluid 3- Recovery Phase: return of kidney function depending on the severity of injury 8

9 Classification AKI is classified according to the physiologic event leading to: Prerenal azotemia Functional, intrinsic Postrenal 9

10 Risk Factors Older age, Higher baseline serum creatinine (SCr), Chronic kidney disease (CKD), Diabetes, Chronic respiratory illness, Underlying cardiovascular disease, Prior heart surgery, Dehydration resulting in oliguria, Acute infection, Renal outflow obstruction, Exposure to nephrotoxins 10

11 Patient Assessment Blood urea nitrogen (BUN) and creatinine guides diagnosis, treatment, and monitoring of AKI. Urinalysis is an important diagnostic tool for differentiating prerenal azotemia, intrinsic, and obstructive AKI. Urinary chemistries are used to differentiate between prerenal azotemia and intrinsic AKI. Microscopic examination of urine helps determine the cause of AKI. 11

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14 Patient Assessment cont. Many equations exist for calculating creatinine clearance (ClCr) or estimated glomerular filtration rate (GFR). Modification of diet in renal disease (MDRD) is used to quantify GFR, to detect or state the stage of CKD, and to follow progression. Estimated GFR (ml/minute/1.73 m2 ) = 170 (SCr) (age in years) (BUN) (Alb) (0.762 if female) (1.18 if black) 15

15 Cockcroft and Gault (CG) equation is used to adjust the doses of medications that are eliminated by the kidney. Estimated ClCr = (140 age inyears)(ideal body weight in kg)/ (72)(SCr in mg/dl) For women, the result is multiplied by 0.85 to account for decreased muscle mass 16

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19 Prerenal AKI results from reduced renal blood flow, with extracellular volume fluid loss and heart failure being the common causes. Functional AKI results from impairment of glomerular ultrafiltrate production or intraglomerular hydrostatic pressure, often caused by medications 20

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22 Intrinsic AKI is seen as damage at the parenchymal level of the kidney. Intrinsic AKI can be divided into: Vascular Glomerular Tubular Dr.Nahid disorder Osman Ahmed 23

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24 Results from outflow obstruction in the urinary tract Common causes are stone formation, underlying malignancies of the cervix or prostrate Onset of symptoms (decreased force of urine stream, dribbling, polyuria) is gradual. Nephrolithiasis (kidney stones) typically present as severe flank pain that radiates to the groin 25

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26 Treatment goals are to minimize further kidney damage and provide symptomatic relief. 27

27 Treatment of the underlying cause of AKI should begin immediately to prevent further kidney damage; currently, there are no drugs that accelerate recovery. Supportive measures are directed at preventing morbidity and mortality. Strict fluid, electrolyte, and nutritional management is important. 28

28 Sodium and water restriction help to reduce edema. Restriction of protein to 0.8 g/kg/day may be beneficial in patients with marked proteinuria. Antihypertensive drugs can be used short term to control blood pressure. 29

29 Diuretics have no role in preventing AKI progression or reducing mortality. Loop diuretics can be used for symptomatic pulmonary or peripheral edema. Intravenous furosemide is preferred ( mg) due to its potency and pulmonary vasodilation properties. Oral furosemide should be avoided. Combinations of loop and thiazide diuretics may be needed in diuretic-resistant disease. 30

30 When possible, use of another imaging study that does not require radiocontrast or use of the lowest dose of a nonionic, iso-osmolar, or lowosmolar agent should be done. Concomitant drug therapy that can impair renal perfusion (e.g., diuretics, [NSAIDs], [ACEIs] inhibitors, [ARBs]) should be discontinued 1 day before and 1 day after radiocontrast administration. 31

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32 For kidney stones: Opiates and NSAIDs, alone or in combination, can be used short term to control pain. Increased fluid intake (2 L daily) is a preventive measure to reduce the likelihood of stone recurrence. Extracorporeal continuous renal replacement therapy (CRRT) is reserved for patients with severe acid base disorders, fluid overload, hyperkalemia, symptomatic uremia, or drug intoxications. 33

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38 Thank you 39