This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student under Nephrology Division under the supervision and administration of Prof. Jamal Al Wakeel, Head of Nephrology Unit, Department of Medicine and Dr. Abdulkareem Al Suwaida, Nephrology Consultant. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

PRESENTED BY: NORA M. AL-BLUWY ACUTE KIDNEY INJURY PRESENTED BY: NORA M. AL-BLUWY

Definition an abrupt or rapid decline in renal filtration function. This condition is usually marked by a rise in serum creatinine concentration or azotemia (a rise in blood urea nitrogen [BUN] concentration). Decreased urine production . Have to exclude other causes of Cr, BUN.

CLASSIFICATION In 2004, the Acute Dialysis Quality Initiative work group set forth a definition and classification system for acute renal failure. Risk of renal dysfunction . Injury to the kidney . Faliure or Loss of kidney function . End stage kidney disease .

Prerenal AKI Volume depletion Renal losses (diuretics, polyuria) GI losses (vomiting, diarrhea) Cutaneous losses (burns, Stevens-Johnson syndrome) Hemorrhage .

Cont.prerenal Decreased cardiac output Heart failure ,Pulmonary embolus Acute myocardial infarction Severe valvular disease .

Cont.prerenal Systemic vasodilatation Sepsis ,Anaphylaxis ,Anesthetics ,Drug overdose Afferent arteriolar vasoconstriction Drugs (NSAIDs, amphotericin B, calcineurin inhibitors, norepinephrine, radiocontrast agents) Hepatorenal syndrome Efferent arteriolar vasodilatation – ACEIs or ARBs

Intrinsic AKI Vascular : Renal artery obstruction : (thrombosis, emboli, dissection, vasculitis) Renal vein obstruction :(thrombosis)

Microangiopathy : (TTP, hemolytic uremic syndrome [HUS], DIC, preeclampsia) Malignant hypertension ,Scleroderma renal crisis . Transplant rejection ,Atheroembolic disease.

Cont.Intrinsic Glomerular Anti–glomerular basement membrane (GBM) disease (Goodpasture syndrome) (ANCA-associated GN) : Wegener granulomatosis, Churg-Strauss syndrome,

Cont.Intrinsic Immune complex GN: lupus, postinfectious, cryoglobulinemia, primary membranoproliferative glomerulonephritis

Cont.Intrinsic Tubular Ischemic Toxic Heme pigment : -rhabdomyolysis -intravascular hemolysis Drugs : aminoglycosides, lithium, amphotericin B pentamidine, cisplatin, ifosfamide, radiocontrast agents)

Cont.Intrinsic Crystals tumor lysis syndrome, seizures, ethylene glycol poisoning, megadose vitamin C, acyclovir, indinavir, Methotrexate.

Cont.Intrinsic Drugs: Interstitial penicillins, cephalosporins, NSAIDs, proton-pump inhibitors, allopurinol, rifampin, indinavir, mesalamine, sulfonamides.

Cont.Intrinsic Infection : Systemic disease : -Pyelonephritis -viral nephritis Systemic disease : Sjögren syndrome, sarcoidosis, lupus, lymphoma, leukemia, tubulonephritis

Postrenal AKI Ureteric obstruction Urethral obstruction stone disease, tumor, fibrosis, ligation during pelvic surgery. Urethral obstruction (strictures, tumor)

Cont.postrenal Bladder neck obstruction : (benign prostatic hypertrophy [BPH], cancer of the prostate [CA prostate or prostatic CA] neurogenic bladder, tricyclic antidepressants, ganglion blockers, bladder tumor, stone disease, hemorrhage/clot)

Frequency United States: 1% of patients , at the time of admission 2-5% during hospitalization. 30 days postoperatively in approximately 1% of general surgery cases.

67% of ICU patients. 95% of consultations with nephrologists are related to AKI.

Mortality/Morbidity The mortality rate estimates for AKI vary from 25-90%. The in-hospital mortality rate is 40-50%; in intensive care settings, the rate is 70-80%.

Clinical History:

Distinguishing AKI from chronic renal failure is important.

A history of chronic symptoms : fatigue, weight loss, anorexia, nocturia, and pruritus . suggests chronic renal failure.

Cont . history Hypotension , Volume contraction , Congestive heart failure . Nephrotoxic drug ingestion ,Toxins. History of trauma or unaccustomed exertion

Cont . history Blood loss or transfusions Evidence of connective tissue disorders or autoimmune diseases Exposure to mercury vapors, lead, cadmium, or other heavy metals, which can be encountered in welders and miners.

People with the following comorbid conditions are at a higher risk for developing AKI: Hypertension . Congestive cardiac failure Diabetes Multiple myeloma Chronic infection Myeloproliferative disorder

Urine output history Oliguria AKI. Abrupt anuria suggests : acute urinary obstruction, acute and severe glomerulonephritis, or embolic renal artery occlusion.

A gradually diminishing urine output may indicate : a urethral stricture or bladder outlet obstruction due to prostate enlargement.

Physical Skin : Petechiae, purpura, ecchymosis, and livedo reticularis provide clues to inflammatory and vascular causes of AKI.

Eyes : Evidence of uveitis : may indicate interstitial nephritis and necrotizing vasculitis.

Cardiovascular system: Pulse rate , BP, JVP, Sacral edema , signs of volume depletion . careful examination of the heart, lungs.

-In hospitalized patients, accurate daily records of fluid intake and urine output and daily measurements of patient weight are important. - Severe hypertension with renal failure suggests renovascular disease, glomerulonephritis, vasculitis, atheroembolic disease.

Abdomen : Abdominal examination : obstruction at the bladder outlet as the cause of renal failure. The presence of an epigastric bruit suggests renal vascular hypertension.

Workup Laboratory Studies:

Prerenal azotemia ATN Inciting factors Low volume Toxins Ischemia medication BUN/creatinine >20/1 <20/1 Urinary Na <20mEq/l >40 FeNa <1 >2 Urine osmolality >500 <350 Urine cells and casts bland Lots of cells, muddy granular, dirty brown casts

In patients who are receiving diuretics, a fractional excretion of urea (FEUrea) can be obtained, since urea transport is not affected by diuretics. The formula for calculating the FEUrea is as follows: FEUrea = (Uurea/Purea) / (UCr/PCr) X 100 FEUrea of less than 35% is suggestive of a prerenal state.

Assessing patient with acute renal failure – Urinary Casts Red cell casts Glomerulonephritis Vasculitis White Cell casts Acute Interstitial nephritis Fatty casts Nephrotic syndrome, Minimal change disease Muddy Brown casts Acute tubular necrosis

Imaging Studies Ultrasonography : Doppler ultrasonography Renal ultrasonography is useful for : evaluating existing renal disease obstruction of the urinary collecting system.  Ultrasonographic scans : small kidneys suggest chronic renal failure. Doppler ultrasonography

Procedures Renal biopsy A renal biopsy can be useful in establishing the diagnosis of intrarenal causes of AKI and can be justified if it will change management (eg, initiation of immunosuppressive medications).

Prolonged abnormal renal function . Acute cellular or humoral rejection in a transplanted kidney can be definitively diagnosed only by performing a renal biopsy.

Treatment of Acute Renal Failure Treat underlying cause: Blood pressure Infections Stop inciting medications Nephrostomy tubes/ureteral stents if obstruction Hydration/diet. Diuresis Dialysis

Indications of dialysis Volume expansion that cannot be managed with diuretics . Hyperkalemia refractory to medical therapy . Correction of severe acid-base disturbances that are refractory to medical therapy .

Pulmonary edema . Uremia, pericarditis . Removal of drugs e.g. lithium .

Key points Aggressive treatment should begin at the earliest indication of renal dysfunction. Correcting acidosis with bicarbonate administration is important.

Maintenance of volume homeostasis and correction of biochemical abnormalities Correcting Hyperkalemia. Correcting hematologic abnormalities.

Complications: Hyperkalemia. Metabolic acidosis . Pulmonary edema. Sepsis . Uremia /encephalopathy. Pericarditis .

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