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The Journey of Kidney Disease

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The Journey of Kidney Disease 2/8/2021 THE JOURNEY OF KIDNEY DISEASE • BY LORETTA DICAMILLO DNP, MSN,RN • RENAL SPECIALISTS • FEBRUARY 6, 2021 FUNCTIONS OF THE KIDNEY The most Vascular organ of the body… Maintenance of body fluids Excretion of wastes Regulation of blood pressure Production of hormones 1 2/8/2021 STATISTICS U.S Department of Health and Human Services More than 726 thousand Americans in 2016 were on dialysis or living with a kidney transplant. Each day over 240 individuals on dialysis pass away. Chronic kidney disease (CKD) is more common in people age 65 and older. 40% of hospitalizations for acute kidney injury (AKI) were among persons with diabetes. The total number of hospitalizations have increased from 900 thousand in the year 2000 to over 3 million in the year 2014. RISKS OF AKI NON-MODIFIABLE MODIFIABLE CHRONIC LIVER DISEASE ANEMIA, HYPERTENSION CONGESTIVE HEART HYPONATREMIA FAILURE, DIABETES HYPOALBUMINEMIA > 65 YEARS OF AGE DRUG USAGE, SEPSIS PERIPHERICAL VASCULAR RHABDOMYOLYSIS DISEASE RENAL ARTERIAL STENOSIS 2 2/8/2021 STAGES OF AKI KDIGO GUIDELINES STAGE 1 STAGE 2 STAGE 3 CREATININE X 1.5 CREATININE X2 CREATININE X 3 BASELINE BASELINE BASELINE OR AN INCREASE TO > 4.0 >0.3 MG/DL URINE OUTPUT < 0.5 MG/DL OLIGURIA < 0.5 MG/KG/HR. FOR > 12 MG/KG/HR. X 6-12 HRS. HRS. ANURIA FOR >12 HRS. BY STAGE THREE PROBABLY NEED RENAL REPLACEMENT THERAPY (RRT) ETIOLOGIES OF AKI PRERENAL – 25% INTRINSIC - 65% PRE-RENAL INTRINSIC POST- ATI- 45% RENAL AKI ON CKD -13% Etiology Hypoperfusion True Kidney Obstruction GN OR VASCULITIS -4% Injury ATHEROEMBOLIC - 1% POSTRENAL – 10% FENa 1% 3.4% Low Yield 3 2/8/2021 PATHOPHYSIOLOGY COMMON ENDPOINT IN ALL TYPES OF ATI IS CELLULAR INSULT SECONDARY TO ISCHEMIA OR DIRECT TOXINS, EFFACEMENT OF THE BRUSH BORDER AND EVENTUALLY CELL DEATH, WHICH SHUTS DOWN THE FUNCTION OF TUBULAR CELLS. INTRATUBULAR OBSTRUCTION PIGMENTS I.E. MYOGLOBIN OR CRYSTALS (URIC ACID) IMMUNOGLOBULIN LIGHT CHAINS SEEN IN MONOCLONAL GAMMOPATHY. INJURY IN GLOMERULONEPHRITIS (GN) MAY BE DIRECT IMMUNE-MEDIATED INJURY OF THE VESSELS OR IMMUNE COMPLEX DEPOSITION LEADING TO IMMUNE RESPONSES AND DAMAGE TO THE GLOMERULI. A 42 YEAR OLD AA FEMALE PRESENTS AS A NEW OUTPATIENT CLINIC ENCOUNTER SHE HAS T2D, HTN, PREVIOUS DEPRESSION AND CHRONIC OSTEOARTHRITIC PAIN. SHE TAKES GLYBURIDE, METFORMIN, HCTZ, METOPROLOL SUCCINATE AND MOTRIN PRN. SHE C/O CHRONIC ARTHRITIC PAIN AND IS DEPRESSED. BP, 160/94 SCR -1.2 MG/DL SNA 135 MMOL/L UA 1+ PROTEIN, NO HEMATURIA SCENARIO YOU START HER ON LOSARTAN AND FLUOXETINE. 4 2/8/2021 ON LAB AND BP FOLLOW –UP, BP 150/84 SCR -1.5 SNA 128 MMOL/L UA1+ PROTEIN, NO HEMATURIA. WHAT CAUSED HER ACUTE KIDNEY INJURY? A. HCTZ B. MORTIN C. LOSARTAN D. ALL OF THE ABOVE SCENARIO DO YOU STOP METFORMIN? (CONT) SCENARIO (CONT) WHAT CAUSED HER AKI? ALL OF THE ABOVE THERE IS INCREASED RISK FOR NSAID INDUCED AKI… ACE & ARB THESE AGENTS CAN REDUCE GFR BY ALTERING INTRARENAL HEMODYNAMICS. DIURETICS ARE R/T KIDNEY HYPOPERFUSION FROM DECREASED INTRAVASCULAR VOLUME. HCTZ THE MOST COMMON CAUSE OF HYPOVOLEMIC HYPOOSMOLALITY ..RENAL SOLUTE LOSS STOP METFORMIN 5 2/8/2021 REVERSIBLE DECREASE IN RENAL PERFUSION RENAL AUTOREGULATION .. ACTIVATION OF REIN ANGIOTENSIN ALDOSTERONE SYSTEM (RAAS) AND ANTI-DIURETIC HORMONE (ADH) LIMITED STRUCTURAL DAMAGE PRERENAL RENAL RESPONSE.. INCREASE IN NA AND H20 AZOTEMIA REABSORPTION ..DECREASE IN URINARY OUTPUT (UO) AND DECREASE IN UREA CLEARANCE PRERENAL AZOTEMIA INTRAVASCULAR VOLUME DEPLETION DECREASED CARDIAC OUTPUT CAUSING DECREASED EFFECTIVE ARTERIAL VOLUME. AND DECREASED CIRCULATING VOLUME. INTERFERENCE WITH RENAL AUTOREGULATION ACE, ARB, NSAIDS This Photo by Unknown Author is licensed under CC BY 6 2/8/2021 PRERENAL AZOTEMIA RENOVASCULAR OBSTRUCTION RENAL ARTERY STENOSIS, THROMBOSIS, DISSECTING ANEURYSM, RENAL VEIN THROMBOSIS, ABDOMINAL COMPARTMENT SYNDROME INCREASED BLOOD VISCOSITY, MULTIPLE MYELOMA, POLYCYTHEMIA INTRINSIC RENAL FAILURE -(ATI) ATI/ATN–THE MOST COMMON CAUSE OF AKI IN HOSPITALIZED PATIENTS WHERE MORTALITY RANGES FROM 40-60% DAMAGE TO THE TUBULAR CELLS, GLOMERULI, INTERSTITIUM TUBULAR DAMAGE ASSOCIATED WITH RELEASE OF VASOCONSTRICTORS FROM THE RENAL AFFERENT PATHWAYS.. PROLONGED RENAL ISCHEMIA , SEPSIS AND NEPHROTOXINS WHICH ARE MOST COMMON ATN.. ISCHEMIA FROM PROLONGED PRERENAL INJURY ACUTE INTERSTITIAL NEPHRITIS (AIN) GLOMERULONEPHRITIS (GN) INTRATUBULAR OBSTRUCTION 7 2/8/2021 CAN OCCUR ANYWHERE IN THE URINARY TACT CONGESTION OF THE FILTRATION SYSTEM LEADING TO A SHIFT IN THE FILTRATION FORCES UNILATERAL OBSTRUCTION MAY NOT ALWAYS PRESENT AS AKI MOST COMMON CAUSES ARE RENAL/URETERAL CALCULI, TUMORS, BLOOD CLOTS, METASTATIC CANCER, BLADDER OUTLET SYNDROME POST-RENAL ETIOLOGY EVALUATION DETAILED EXAM ..ORTHOSTATIC VITAL SIGNS, EDEMA, INTAKE OF FLUIDS, INFECTION, COLOR OF URINE, IV CONTRAST THE TIMING OF THE ONSET OF AKI SKIN; LIVEDO RETICULARIS, BUTTERFLY RASH, TRACK MARKS EYES, EARS. JAUNDICE, BAND KERATOPATHY, ATHEROEMBOLI IN RETINOPATHY, UVEITIS, HEARING LOSS IN ALPORT DISEASE IRREGULAR RHYTHM, PERICARDIAL FRICTION RUB 8 2/8/2021 EVALUATION LABS MAY INCLUDE BNP, RENAL PANEL, URINE ELECTROLYTE, URINE PROTEIN, URINE OSMOLALITY, URINE ALBUMIN TO CREATININE RATIO, SERUM ALBUMIN URINE AND SERUM PROTEIN ELECTROPHORESIS (SPEP) TO RULE OUT MONOCLONAL GAMMOPATHY OR MULTIPLE MYELOMA RENAL ULTRASOUND OR CT NON-CONTRAST URINE SEDIMENT WITH MUDDY BROWN CASTS OR STERILE PYURIA RBC CASTS BIOPSY EVALUATION MARKERS FOR TUBULAR FUNCTION TO HELP WITH PRERENAL AND INTRARENAL/POSTRENAL FRACTIONAL EXCRETION OF SODIUM (FENA) > 2% OR <1% FRACTIONAL EXCRETION OF UREA (FEUREA) < 35% OR > 35% BLOOD UREA NITROGEN TO SERUM CREATININE RATIO 20:1 OR 10:1 URINE SODIUM (UNA) >20 OR < 20 ASSESS VOLUME STATUS TO R/O CARDIORENAL OR HEPATORENAL SYNDROME. 9 2/8/2021 HIGH DEGREE OF ACCURACY IN DIFFERENTIATING BETWEEN REVERSIBLE PRERENAL AND ATN THE RATIO % = FILTERED SODIUM EXCRETED IN THE URINE/AMOUNT OF NA FILTERED THROUGH THE KIDNEY FENA UNA X SCR = ----------- X100 FRACTIONAL SNA X UCR EXCRETION OF SODIUM FENA <1% SUGGESTS PRERENAL, AS SODIUM IS BEING REABSORBED IN RESPONSE TO DECREASED RENAL PERFUSION AND GFR IS PRESERVED FENA <1% CAN OCCUR WITH SEPSIS, MALIGNANT HTN, COMPARTMENT SYNDROME, CHF, CIRRHOSIS, ACUTE GLOMERULONEPHRITIS, FROM AFFERENT ARTERIOLAR CONSTRICTION, BILATERAL ARTERY STENOSIS, BURNS, RENAL FRACTIONAL TRANSPLANT REJECTION EXCRETION OF SODIUM 10 2/8/2021 FRACTIONAL EXCRETION OF SODIUM FENA >2% USUALLY INDICATES ATN…TUBULAR DYSFUNCTION WITH INABILITY TO CONSERVE NA. CONSISTENT WITH VOLUME DEPLETION IN PATIENTS RECEIVING DIURETICS OR IN PATIENTS WITH CHRONIC KIDNEY DISEASE DUE TO IMPAIRED SODIUM REABSORPTION. COMPLICATIONS OF AKI ANEMIA, PLATELET FLUID OVERLOAD DYSFUNCTION HYPERKALEMIA IMMUNE DYSFUNCTION, PERICARDITIS DECREASED CARDIAC OUTPUT, LV DILATION, APOPTOSIS SEVERE METABOLIC ACIDOSIS (PH<7.1) IMPAIRED MOBILITY, EDEMA ACUTE LUNG INJURY AND BRAIN PANCREATITIS, COLITIS, INFLAMMATION FROM UREMIC BURDEN METABOLIC INSULIN MYOPATHY, ENCEPHALOPATHY RESISTANCE, HYPERLIPIDEMIA HEPATOCYTE INJURY 11 2/8/2021 TREATMENT OF AKI VOLUME RESUSCITATION DIURETICS MAY BE REQUIRED DURING THE OLIGURIC PHASE OF ATI IF SIGNIFICANT VOLUME GIVE IV FLUID CHALLENGE UNLESS OVERLOAD DEVELOPS. CONTRAINDICATED CRYSTALLOIDS.. ISOTONIC MONITOR FOR START 1-3 LITERS, 5L WITH BURNS AND HYPERCHLOREMIA AND RENAL PANCREATITIS VASOCONSTRICTION, COLLOIDS MORE EXPENSIVE AKI, HYPERVOLEMIA, NOT ANURIC AND ADDITIONAL BENEFIT IS QUESTIONABLE FUROSEMIDE 80 MG UP TO A SINGLE BUFFERED SOLN I.E. LACTATED RINGERS MORE DOSE 200 MG. PH. BALANCE, NO HYPERCHLOREMIA, BUT AVOID OVERAGGRESSIVE FLUID POTASSIUM CAN BE A PROBLEM REPLACEMENT IN PATIENTS WITH VASOPRESSORS FOR HYPOTENSION DESPITE SEPSIS FLUID RESUSCITATION 70-75 % OF TIME ARE FROM MEDICATIONS ANTIBIOTICS 30-50%.. PCN, SULFONAMIDES, QUINOLONES (ESP CIPRO), INH, RIFAMPIN, VANCOMYCIN LATENCY – ONE TO TWO WEEKS UNLESS PREVIOUSLY SENSITIZED SUGGESTS T CELL MEDIATION; MOSTLY T CELL INTERSTITIAL INFILTRATES ON RENAL BX NSAIDS, COX2 INHIBITORS, PPI’S, DIURETICS, PHENYTOIN, ALLOPURINOL, ACYCLOVIR, ALLERGIC AMLODIPINE, DILTIAZEM, CIMETIDINE, COCAINE. LUPUS, SJOGREN, SARCOIDOSIS, HEP C, HIV, INTERSTITIAL STREP, STAPH, ASSOCIATED WITH AIN NEPHRITIS 12 2/8/2021 ALLERGIC INTERSTITIAL NEPHRITIS PRESENT WITH ACUTE OR SUBACUTE ONSET OF N/V, MALAISE, MANY ASYMPTOMATIC FEVER 27%, RASH 15%, EOSINOPHILIA 23% STERILE PYURIA, WBC CASTS, HEMATURIA WITHOUT RBC CASTS, PROTEINURIA <1G OFTEN REVERSIBLE WITH WITHDRAWAL OF OFFENDING MEDICATION OR TREATMENT OF THE UNDERLYING DISEASE. CORTICOSTEROIDS ROLE REMAIN CONTROVERSIAL, AVAILABLE DATA IS CONFLICTING, NO CONTROL TRIAL. COULD CONSIDER A SHORT COURSE IF WITHOUT IMPROVEMENT AFTER 3-10 DAYS OF D/C THE OFFENDING AGENT. SCENARIO A 50 YEAR OLD ALCOHOLIC MALE PRESENTS WITH SEPSIS SECONDARY TO KLEBSIELLA PN. HIS BACKGROUND INCLUDES PREVIOUS PN , HTN, HIGH CHOLESTEROL. MEDICATION INCLUDES FUROSEMIDE, ENALAPRIL, ASA, CLOPIDOGREL, SIMVASTATIN, AMOXICILLIN. PT IS IN ICU FOR 1 WK. ON STEP DOWN TO MEDICAL UNIT LABS REVEAL SODIUM 132, K+ 5.0, UREA 24 FROM 8 AND CREATININE 3.9 FROM 0.6. BP 135/83, HR 90 HE IS CATHETERIZED WITH U/O 35 ML/HR. 13 2/8/2021 SCENARIO WHICH TX IS BEST? SWITCH TO HIGH DOSE IV FUROSEMIDE, STOP ENALAPRIL, GIVE IV FLUIDS TO MAINTAIN URINE OP, DAILY LABS STOP FUROSEMIDE, STOP ENALAPRIL, ADD IN DOPAMINE AND MAINTAIN ADEQUATE HYDRATION TO MAINTAIN URINE OUTPUT, LABS STOP FUROSEMIDE, STOP ENALAPRIL, ADEQUATE FLUIDS TO MAINTAIN URINE OUTPUT, LABS CONTINUE FUROSEMIDE, STOP ENALAPRIL, HIGH DOSE CORTICOSTEROIDS AND CONTINUE ADEQUATE
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