Acute Kidney Injury (AKI)

Transcription

1 (Last Updated: 08/22/2018) Created by: Socco, Samantha Acute Kidney Injury (AKI) Thambi, M. (2017). Acute Kidney Injury. Lecture presented at PHAR 503 Lecture in UIC College of Pharmacy, Chicago. AKI This is an acute decline in kidney function, whereas CKD must be renal dysfunction for >/= 3 months Non-preventable risk factor for AKI: o An AKI on top of CKD o Being older than 75 y/o o Having peripheral vascular disease o Heart failure o Liver disease o Diabetes Preventable risk factors for AKI o Nephrotoxins NSAIDs Aminoglycosides o Hypotension o Sepsis tx with antibiotics early enough, it s preventable Usually asymptomatic but can begin to show symptoms of CKD o Edema, increase in K +, Magnesium, Phosphate o Acidosis o High BUN TYPES OF AKI: PRE-RENAL Pre-renal = not enough blood getting to the kidney ischemia (kidney cells die) o Intravascular volume depletion Hypovolemia (dehydration) Hemorrhage GI loss (diarrhea/vomit) Frequent urination (thiazide + loop diuretic) Decreased effective volume = can t keep blood in vasculature (escaping into interstitium) cirrhosis, CHF

2 Peripheral vasodilation = shunting from kidney to periphery o Reduced cardiac output Hypotension HF (heart failure) MI (myocardial infarction) Certain drugs (calcium channel blockers) o Vascular obstruction Bilateral renal artery stenosis = closing off of the renal arteries Afferent arteriole vasoconstriction NSAIDs Epinephrine/norepinephrine Tacrolimus, cyclosporine (transplant drugs) o Diagnosis: History (did pt. get thiazide + loop diuretic?). is pt. dehydrated? Physical exam (orthostatic hypotension get dizzy when standing up) Dehydration = poor skin turgor Give fluids, if SCr gets better, then it s probably pre-renal, if not then it s probably intrinsic Labs BUN:SCr > 20 = dehydration Urine specific gravity > Urine osmolality > 500 Urine Na + <20 Na + low b/c body trying to keep Na + in to keep water Fractional excretion of Na + <1% (DIFFERENTIATES between pre-renal AKI and intrinsic AKI) o Excreted (filtered reabsorbed) / filtered o <1 % = pre-renal AKI o 1-2% = either pre-renal or intrinsic o > 2% = intrinsic AKI o Be careful: may not be accurate if pt. is urinating frequently (>500 ml/d) or on diuretics (use FEUrea instead) FEUrea < 35% = pre-renal AKI FEUrea 50-65% = intrinsic AKI o Progression of pre-renal AKI Get less blood flowing to kidney compensate by decreasing Na + output and activation RAAS (renin angiotensin aldosterone system) 2

3 get increase in aldosterone and ADH less urine output, less Na + excretion get highly concentrated urine with low Na + o Treating pre-renal AKI Hypovolemia = re-hydrate with ml bolus of 0.9% NaCl or Lactated Ringers (LR) and/or maintenance dose 35 ml/kg/day DON T use dextrose TYPES OF AKI: INTRINSIC Intrinsic = direct damage to the kidney itself (tubules, glomerulus, interstitial fluid) o Causes: Prolonged pre-renal AKI Prolonged post-renal AKI = urine backs up, nephrons are pressure sensitive Acute tubular necrosis (ATN) = sudden hypotension/ischemia Acute interstitial nephritis drug allergy or auto-immune induced (pt. may get rash and fever) Acute glomerulonephropathies (GNs)= usually drug-induced or autoimmune Pt usually has proteinuria = urine protein > 3.5 gm/d Get inflammation (proteins damage the tubules) nephritic syndrome Quantification done with 24 hr urine collection or spot albumin:creatinine ratio o Albumin:creatinine ratio is sensitive but not specific Nephrotic syndrome (different than Nephritic syndrome) = signs/symptoms seen in pt with proteinuria o Edema = losing albumin and cant keep volume in vasculature b/c of the decrease in oncotic pressure o Urine will look frothy o Ramped up protein production cholesterol production o Less antithrombin = higher risk for blood clots o Less complement protein and antibodies = higher risk infection Nephritic syndrome (different than nephrotic syndrome) = intraglomerular inflammation basically at end stage renal disease 3

4 o Will have all symptoms of nephrotic syndrome but also: Hematuria (RBCs are casted or dysmorphic) Oliguria Less CrCl Hypertension How to treat GNs: o Immunosuppressive therapy o Tx the proteinuria Increase dietary intake Use an ACEI (Angiotensinogen converting enzyme inhibitor) or ARB (angiotensin receptor blocker) w/ low salt diet o Tx hyperlipidemia (lifestyle mods) o Tx hypertension (ACEIs or ARBs) o Tx blood clots Anticoagulation only do this if they get a clot Acute = inpatient heparin Outpatient: warfarin or low molecular weight heparin o Tx edema Sodium restriction (<2 gm/day) Can try loop diuretics if really bad o When to start dialysis: AEIOU A = metabolic Acidosis (ph < 7.1) E = Electrolytes (K + > 6.5) I = Intoxication O = Refractory fluid Overload U = Uremia (person will be confused) Starting early will not improve outcomes however Types of dialysis (see dialysis study guide as well) Intermittent hemodialysis or peritoneal dialysis Continuous renal replacement therapy (CRRT) 4

5 TYPES OF AKI: POST-RENAL Post-renal = obstructing urine outflow to bladder or urethra o This causes urine to backup (hydronephrosis) more pressure on nephrons interstitial damage and risk of UTI (urinary tract infection) or pyelonephritis (infection of the kidneys) o Caused by: Congenital problems from childhood Calculi = kidney stones Benign prostatic hyperplasia (BPH) or prostate cancer usually in older men o Urolithiasis = stones that form in urinary system Nephrolithiasis = stones in kidney Ureterolithiasis = stones in ureters Pathophysiology: Build up of calcium/oxalate salts get crystal formation damages ureters crystals grow there recurrence from remnants Most made of calcium oxalate or calcium phosphate Some made of uric acid, struvite (magnesium ammonium phosphate diuretics increase risk of this), or cystine Risk factors: Diabetes, obesity, gout, HTN, previous kidney stone, hyperparathyroidism, family hx, bariatric surgery Low fluids, high salt diet, high protein diet, high sugar diet, drinking soda (phosphoric acid) Certain medications: ex.) loop diuretics Symptoms Asymptomatic Renal colic = spasm of the ureters Pain that waxes and wanes If stones > 10 mm, probably not going to pass on their own Medical expulsive therapy (MET) o Use tamsulosin (highest evidence), nifedipine, or tadalafil If stones < 5 mm can let pass on their own and hydrate the pt while controlling their pain Preventing stones: 5

6 Increase fluid intake and avoid dark sodas w/ phosphoric acid while keeping low sodium diet. Other ways have little evidence Using thiazide diuretics and potassium citrate DON T: take Vit. C, lower calcium in diet, or take calcium supplement 6