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

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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 FAILURE, DIABETES HYPOALBUMINEMIA > 65 YEARS OF AGE DRUG USAGE, SEPSIS PERIPHERICAL VASCULAR RHABDOMYOLYSIS DISEASE RENAL ARTERIAL STENOSIS

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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

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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.

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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

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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

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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

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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

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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.

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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

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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   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, HEPATOCYTE INJURY

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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 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

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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.

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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 FLUIDS TO MAINTAIN URINE OUTPUT , DAILY LABS

HYPERKALEMIA

FROM OLIGURIA WITH HIGHLY CATABOLIC STATES, CRUSH INJURIES, TUMOR LYSIS, GI BLEEDS 10-20 ML OF CALCIUM GLUCONATE 10% SOLN OVER 2-3 MIN CALCIUM: THE EFFECT WITHIN MINUTES, BUT ONLY LAST 3-6- MINUTES INSULIN REGULAR 10 UNITS IV WITH 50 ML OF 50% GLUCOSE ALBUTEROL (VENTOLIN 10-20 MG BY NEBULIZER OVER 10 MINUTES BICARBONATE IV 50 MEQ OVER 5 MIN SODIUM POLYSTYRENE SULFONATE (KAYEXALATE) 50 G IN 30 ML SOLN RRT PRN DO NO UTILIZE VELTASSA DUE TO ITS DELAYED ONSET

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METABOLIC ACIDOSIS

AKI IMPAIRED EXCRETION OF DAILY ACID LOAD (H+) AND BICARBONATE REGENERATION/LOSS. SEPSIS, TRAUMA, MULTI-ORGAN FAILURE TREAT WHEN PH. < 7.1 HEMODYNAMIC INSTABILITY, DECREASED RESPONSE TO CATECHOLAMINES/VASOPRESSORS, DECREASED CARDIAC OUTPUT, ARRHYTHMIAS, ARTERIAL VASODILATION IV BICARB 2-5 MEQ/KG OVER 4-8 HRS. ACHIEVE TARGET OF PH. OF 7.2 CAN CAUSE .. DECREASES IONIZED CA.. CAUSE SEIZURES. CORRECT HYPOCALCEMIA RENAL REPLACEMENT THERAPY (RRT ) IF OLIGURIA OR ANURIA AND VOLUME OVERLOAD

AKI-CORONAVIRUS DISEASE 2019 (COVID-19)

MULTIFACTORIAL SYSTEMIC IMMUNE AND INFLAMMATORY RESPONSES MORTALITY IS HIGH 35% - 46% HAVE SOME FORM OF PERSISTENT KIDNEY DYSFUNCTION OTHER COMORBIDITIES.. DM, HTN CAD, OBESITY, CVD, ELDERLY, CKD CLINICAL PRESENTATION.. FEVER, COUGH, DYSPNEA, CHILLS MYALGIA, GI SXS, HYPOSMIA, DYSGEUSIA, OLIGURIA MOST PATIENT WITH AKI AND COVID-19 APPEARS TO BE MAINLY ATN INJURY. PROTEINURIA > 2+ AND HEMATURIA ARE COMMON

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AKI-COVID -19

MITOCHONDRIA PLAYS A CENTRAL ROLE IN METABOLIC DEREGULATION AND ADAPTIVE RESPONSE TO THE SYSTEMIC INFLAMMATION. THERE MAY BE A LINK WITH THE EPITHELIAL CELLS THAT EXPRESS ACE2 RECEPTORS FINDING OF AKI WERE SEVERE HYPOXEMIA, LATE CARDIAC INVOLVEMENT, SYSTEMIC HYPERINFLAMMATION, HYPERCOAGULABLE STATE, DAMAGE ASSOCIATED MOLECULAR PATTERNS (DAMP) RIGOROUS INFLAMMATION REACTION REDUCTION IN PLATELETS AND ENDOTHELIAL CELLS

AKI-COVID -19

AFFECTED LABS, D-DIMER, ,CRP, IL-6, WBC, PLT, URINALYSIS, SCR, GFR, ELECTROLYTES, PHOSPHATES, FIBRINOGEN, H& H, LIVER ENZYMES, ALBUMIN, FERRITIN TREATMENT IS SIMILAR TO SEPTIC SHOCK-RELATED AKI, ADMISSION TO ICU, USE OF FLUID MANAGEMENT, VASOPRESSORS, MECHANICAL VENTILATION, ABX, ANTICOAGULATION, RENAL REPLACEMENT THERAPY (RRT), OTHER TX… REMDESIVIR, HYDROXYCHLOROQUINE

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OLIGURIA REFRACTORY HYPERKALEMIA, DIURETIC RESISTANT, FLUID OVERLOAD, METABOLIC ACIDOSIS – PH < 7.1 WITH VOLUME OVERLOAD UNABLE TO TOLERATE SODIUM LOAD FROM BICARBONATE. EXOGENOUS TOXINS.. LITHIUM, ALCOHOLS, SALICYLATES, THEOPHYLLINE NON-EMERGENT UREMIA WITH PERICARDITIS, ENCEPHALOPATHY, PROLONGED AKI USUALLY IF BUN > 100MG/DL FOR FEW DAYS TREATMENT OF RANDOMIZED, CONTROLLED TRIALS COMPARING AKI WITH RRT EARLY VERSUS DELAYED INITIATION OF RRT HAVE NOT DEMONSTRATED BENEFIT WITH EARLIER INITIATION OF RRT

AN 85 YEAR-OLD MALE PRESENTS TO THE EMERGENCY ROOM WITH PNEUMONIA. HE HAS BEEN FEBRILE FOR SEVERAL DAYS AND HAS HAD A COUGH PRODUCTIVE OF YELLOW SPUTUM. ON PHYSICAL EXAM HE IS A WELL-DEVELOPED, THIN MALE IN MODERATE RESPIRATORY DISTRESS. BLOOD PRESSURE (SUPINE) 120/86, PULSE 74, BLOOD PRESSURE (STANDING) 115/85, PULSE 70, RESPIRATIONS 24 AND LABORED. TEMPERATURE WAS 39OC. BODYWEIGHT 60 KG. HEENT EXAM WAS UNREMARKABLE. CARDIOPULMONARY EXAM DEMONSTRATED DECREASED BREATH SOUNDS AT THE BASE OF THE RIGHT LUNG. UNA 60 MMOL/UK+ 30 MMOL/L, UOSMOL 500 MOSM/KG, SNA120 , SK 3.9 +, SCL 87, SC02 24, SBUN 10, SCR 0.8MG/DL, GLUCOSE , 90 SOSM 248 SCENARIO

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SCENARIO

WHAT IS THE CAUSE OF HYPONATREMIA IN THIS PATIENT? BASED ON WHAT CRITERIA WAS THIS DIAGNOSIS MADE? WHAT IS THE TOTAL BODY SODIUM IN THIS PATIENT? IF FUROSEMIDE IS ADMINISTERED HOW WILL IT CHANGE THE URINARY COMPOSITION.

HYPONATREMIA

 MILD SODIUM < 135 MMOL/L REMEMBER HYPONATREMIA IS AN IMBALANCE IN THE RATIO WHERE TOTAL  MODERATE SODIUM 120-129 BODY WATER IS MORE THAN TOTAL MMOL/L BODY SOLUTES.  SEVERE SODIUM < 120 MMOL/L IT’S ALL ABOUT H20.  SXS ARE ANOREXIA, N/V THIRST STIMULATION, ADH AND FATIGUE, HA, MUSCLE CRAMPS , FILTERED NA BY KIDNEYS REGULATE AMS, AGITATION, SEIZURES AND SERUM NA AND OSMOLALITY. COMA. HYPERTONIC HYPONATREMIA ISOTONIC HYPONATREMIA 

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TREATMENT DEPENDS UPON THE DEGREE, DURATION AND SEVERITY OF SXS AND VOLUME STATUS. EMERGENT TREATMENT INDICATED.. THOSE WITH RISK FOR LIFE THREATING CEREBRAL EDEMA WITH BRAIN HERNIATION I.E MARATHON RUNNERS, PSYCHOGENIC POLYDIPSIA, ECSTASY. ACUTE < 48 HRS WITH SEVERE SXS WANT TO INCREASE NA BY 4-6 MEQ OVER FEW HRS HYPONATREMIA

HYPONATREMIA

CHRONIC HYPONATREMIA CORRECT NA BY NO MORE THEN 10 MEQ/L-12MEQ/L IN FIRST 24 HRS AND 18 MEQ/L IN THE FIRST 48 HRS. HIGH RISK FOR ODS >8 MEQ/L IN 24 HRS AVERAGE RISK FOR ODS > 10MEQ/L IN 24 HRS HYPOVOLEMIC HYPONATREMIA: ISOTONIC FLUIDS AND HOLD DIURETICS HYPERVOLEMIC HYPONATREMIA: RESTRICT SALT AND FLUIDS AND GIVE LOOP DIURETIC EUVOLEMIC HYPONATREMIA : FLUID RESTRICTION TO < 1 LITER PER DAY

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OSMOTIC DEMYELINATION SYNDROME

INCREASED RISK FOR OSMOTIC DEMYELINATION SYNDROME (ODS) WITH OVER-RAPID CORRECTION OF HYPONATREMIA .. HYPOXEMIA IMPAIRED BRAIN ADAPTATION NA <105 MEQ/L RISKS: HYPOKALEMIA, ALCOHOLISM, MALNUTRITION, LIVER DISEASE, PROLONGED DIURETIC USAGE HOSPITALIZE IF: ACUTE OR HYPERACUTE, MOST WITH SEVERE, AND MANY WITH MODERATE SXS, SEIZURES

EVALUATION OF HYPONATREMIA IN STABLE PATIENT

CHECK GLUCOSE, CALCULATE LOW SOLUTE “TEA AND TOAST”, HIGH CORRECTED SODIUM FLUID/LOW SOLUTE “BEER CHECK HYPO-OSMOLAR STATE POTOMANIA, PSYCHOGENIC POLYDIPSIA APPROPRIATE DILUTE < 100 MOSM/KG SIADH EVALUATION DISCONTINUE THIAZIDE AND GIVE ONE WEEK TO CORRECT TSH, BUT IF ELEVATED, DO NOT PRESUME IT’S THE CAUSE ? CHF, CIRRHOSIS LOW BP CHECK CORTISOL LEVELS, ? DIARRHEA, VOMITING ..CHECK UNA, TEST FOR ADRENAL INSUFFICIENCY UCL, UCR CHECK MEDS .. DIURETIC, NSAIDS

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OFFICE MANAGEMENT OF CHRONIC MODERATE HYPONATREMIA

HF, CIRRHOSIS, SIADH, POLYDIPSIA ..RESTRICT FLUID < 1 LITER/DAY. CAN ADD LOW DOSE LASIX 10-20 MG BID LATER, ADD SALT TABLETS - 3 TO 9 GM/DAY DEMECLOCYCLINE. DECREASE TUBULAR RESPONSIVENESS TO ADH .. 300 TO 600 MG BID. TAKE A FEW DAYS TO WORK TOLVAPTAN V2 RECEPTOR ANTAGONIST .. MAX USAGE IS 30 DAYS: DON’T GIVE WITH LIVER DISEASE IF WITH TRUE VOLUME DEPLETION.. ISOTONIC SALINE WILL TURN OFF ADH

 MOST COMMON CAUSE OF OUTPATIENT HYPONATREMIA.  MOST OFTEN IN THE ELDERLY, FEMALES AND THOSE WITH LOW BODY MASS.  DUE TO NA AND K EXCRETION AND ENHANCED WATER REABSORPTION (DUE TO ADH).  HYPONATREMIA MORE OF A RISK WITH WATER REABSORPTION VIA AQUAPORIN-2 CHANNELS  TREATMENT OF DIURETIC –INDUCED HYPONATREMIA .. DISCONTINUE, ADMINISTER EITHER ISOTONIC OR HYPERTONIC SALINE.  TO ASSESS RESPONSE OF SALINE INFUSION 1-2 LITERS.. ADH WILL BECOME SUPPRESSED, URINE BECOMES THIAZIDE DILUTE AND NA INCREASES. DIURETICS

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SSRI’S INDUCED HYPONATREMIA

 SECOND MOST COMMON CAUSE OF DRUG-INDUCED HYPONATREMIA.  85% > 60 YEARS OLD  OCCURS WITH ALL SSRI’S  SERTRALINE 42% PAROXETINE 15% FLUOXETINE 15%  MEDIAN TIME TO ONSET IS 13 DAYS  ATTRIBUTED TO NON-BARORECEPTOR MEDIATED INCREASED ADH RELEASE  HIGHER RISK FOR HYPONATREMIA ARE ELDERLY INDIVIDUALS WITH LOW BMI, HCTZ AND NSAIDS’.

CAUSES OF CKD

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CHRONIC KIDNEY DISEASE

 STAGE 1 GFR NORMAL OR HIGH- >90 ML/MIN  STAGE 5 KIDNEY FAILURE <15 ML/MIN  STAGE 2 GFR MILD DECREASE - 60-89  ALBUMINURIA/24H CATEGORIES IN CKD  STAGE 3A GFR MILD TO MODERATE  A1 NORMAL TO MILDLY INCREASED DECREASE 45-59 ML/MIN <30 MG/DAY  STAGE 3B GFR MODERATE TO SEVERE  A2 MODERATELY INCREASE 30-300MG/ DECREASE 30-44 ML/MIN  STAGE 4 GFR SEVERE DECREASE 15-29  A3 SEVERELY INCREASE > 300 MG/DAY

ASSESSING RENAL FUNCTION

ESTIMATE GLOMERULAR FILTRATION RATE (GFR) NORMAL – 90-120 ML/MIN GFR DECREASE BY 1 ML/MIN AFTER THE AGE OF 35 IN MANY  DUE TO GLOMERULAR DETERIORATION WITH AGE. CURRENTLY, USE CREATININE CLEARANCE TO ESTIMATE GFR UTILIZING THE MODIFICATION OF DIET IN RENAL DISEASE (MDRD) CREATININE IS FREELY FILTERED CREATININE SECRETED BY PROXIMAL TUBULES ORGANIC CATION SECRETORY PATHWAYS CIMETIDINE, FENOFIBRATES AND STEROIDS CAN INCREASE SCR

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EACH DOUBLING OF CREATININE HALVES THE GFR SCR 1-2 GFR 100-50 ML/MIN SCR 2-4 50-25 ML/MIN SCR 4-8 25-10 ML/MIN NEPHRON LOSS AND GFR ARE NOT LINEAR.. AS REMAINING GLOMERULI UNDERGO HYPERTROPHY AND COMPENSATORY HYPERFILTRATION. E.G A PATIENT WHO DONATES A KIDNEY USUALLY SERUM HAS A GFR > 50ML/MIN CREATININE

PREFERRED SCREENING STRATEGY IN DIABETICS NORMAL PCR IS < 0.2 MG/DL NORMAL ACR < 30 MG/DAY NEED TO REPEAT >2 X OVER 3-6 MONTHS TO CONFIRM PERSISTENCE URINE PATIENT SHOULD REFRAIN FROM VIGOROUS PROTEIN/CREATINE EXERCISE IN 24 HRS PRIOR TO THE TEST RATIO (PCR) BEST PREDICTIVE VALUE FOR RENAL DISEASE URINE PROGRESSION ALB/CREATININE IF PT WITH MODERATE OR SEVERE ALBUMINURIA RATIO (ACR) START ACE OR ARB

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THE GOLD STANDARD FOR MEASUREMENT OF PROTEIN EXCRETION NORMAL IS LESS THAN 150MG/DAY SHOULD BE PERFORMED IN PATIENTS WITH PERSISTENT PROTEINURIA. GET A 24 HR URINE CREATININE ALONG WITH PROTEIN CHECK FOR ADEQUACY OF COLLECTION  MEN EXCRETE 20 TO 25 MG/KG OF CREATININE  WOMEN EXCRETE 16 TO 20 MG/KG OF CREATININE 24 HOUR URINE  PROTEINURIA PROTEIN  < 1 G/DAY IS MILD QUANTITATION  1-3 G/DAY IS MODERATE  > 3.5 G/DAY IS NEPHROTIC RANGE

PROTEINURIA/HEMATURIA

SUGGESTIVE OF GLOMERULAR DISEASE (GN) SEROLOGIC EVALUATION INCLUDES ANA, ANTI-DSDNA, C3,C4, SPEP, SICKLE CELL/TRAIT, ANTI-PLA2R AUTO- ANTIBODY, ANTI-GBM ANTIBODIES, ANTI-PROTEINASE-3 ANTIBODIES (PR3), ANCA GENETIC TESTING • IMPORTANT TO DIAGNOSE PROMPTLY AS ADMINISTRATION OF IMMUNOSUPPRESSIVES, PLASMA EXCHANGE OR BOTH ARE IMPERATIVE

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WHEN TO REFER/CALL NEPHROLOGY

 GFR DECLINE OF > 30% IN LESS THAN 4 MONTHS WITHOUT CAUSE  GFR DECLINE OF >30% AFTER STARTING AND ACE OR ARB  RAPIDLY DECLINING GFR • ACUTE ONSET NEPHROTIC SYNDROME OR RAPIDLY INCREASING PROTEINURIA > 3.5G/DAY OF UNKNOWN CAUSE  ACUTE NEPHRITIS >>GLOMERULAR HEMATURIA WITH RBC CASTS OR OTHER CELLULAR CASTS  AKI WITH NON –UROLOGIC HEMATURIA  RESISTANT/REFRACTORY HTN (ON OPTIMAL DOSES OF 3 ANTI- HYPERTENSIVES)  URGENT IF SCR INCREASED 20% OR OVER 3.39 MG/DL OVER A SHORT PERIOD OF TIME  ROUTINE CONSULT WHEN GFR < 50ML/MIN

THE JOURNEY OF KIDNEY DISEASE

QUESTIONS?

• BY LORETTA DICAMILLO DNP, MSN,RN • RENAL SPECIALISTS • FEBRUARY 6, 2021

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REFERENCES

AMERICAN SOCIETY OF NEPHROLOGY. HTTPS://JASN.ASNJOURNALS.ORG SCOTT ET AL. (2018). PRIMER ON KIDNEY DISEASES. PHILADELPHIA: ELSEVIER. WWW.CDC.GOV/CKD (2020) WWW.UPTODATE. (2021)

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