ALL ABOUT INTERNAL MEDICINE (AAIM)
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AZOTEMIA AND URINARY ABNORMALITIES
HARRISON’S PRINCPLES OF INTERNAL MEDICINE 17TH EDITION
CHAPTER 45, PAGE 268 - 274
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ANATOMY
RENAL CORPUSCLE
RENAL TUBULE & MEDULLARY RAYS COLLECTING
DUCT RENAL PAPILLA
MINOR & MINOR CALYCES
RENAL PELVIS
URETER
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ANATOMY
S RETROPERITONEAL AREA – OBLIQUE ANGLE
S ASYMMETRIC LOCATION S RIGHT KIDNEY :
S LOWER THAN THE LEFT, SITS BELOW THE DIAPHRAGM AND POSTERIOR TO THE LIVER
S LEFT KIDNEY : S MORE MEDIAL THAN THE RIGHT, T12 – L3,
POSTERIOR TO THE SPLEEN, TYPICALLY LARGER THAN THE RIGHT
S WEIGHTS : S MALE : 125 – 170 GRAMS S FEMALES : 115 – 155 GRAMS
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ANATOMY
S SIZE : 11 – 14 CM X 6 CM X 4 CM
S PARENCHYMA : S SUPERFICIAL – RENAL CORTEX S PROFUNDA (DEEP) – RENAL MEDULA
S 8 – 18 CONE SHAPED RENAL LOBES S RENAL PYRAMID (OF MALPIGHI) S RENAL COLUMNS (OF BERTIN)
S NEPHRONS : S URINE PRODUCING FUNCTIONAL STRUCTURES
OF THE KIDNEY
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NEPHRONS
URINE PRODUCING FUNCTIONAL STRUCTURES OF THE KIDNEY
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NEPHRONS
Efferent Arteriole
Afferent Arteriole
Juxtaglomerular Cell
Pedicel
Podocyte
Parietal Layer Of The Bowman’s Capsule
Proximal Convoluted Tubules
Capsular Space
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PHYSIOLOGY
S WHOLE BODY HOMEOSTASIS S REGULATING ACID – BASE BALANCE S ELECTROLYTE CONCENTRATIONS S EXTRACELLULAR FLUID VOLUME S REGULATION OF BLOOD PRESSURE S HORMONE SECRETION S EXCRETION OF WASTES
S MECHANISM : S FILTRATION, REABSORPTION, AND
SECRETION
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CLINICAL MANIFESTATION
S DISTURBANCES IN URINE VOLUME S OLIGURIA, ANURIA, POLYURIA
S ABNORMALITIES OF URINE SEDIMENT S RBC, WBC, CASTS, CRYSTALS
S ABNORMAL EXCRETION OF S. PROTEIN (PROTEINURIA)
S REDUCTION IN GFR (AZOTEMIA)
S PRESENCE OF HYPERTENSION AND / OR EXPANDED TOTAL BODY FLUID VOLUME (EDEMA)
S ELECTROLYTE ABNORMALITIES
S FEVER / PAIN
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CLINICAL MANIFESTATION S DISTURBANCES IN URINE VOLUME (OLIGURIA, ANURIA,
POLYURIA)
S ABNORMALITIES OF URINE SEDIMENT S RED BLOOD CELLS (RBC) S WHITE BLOOD CELLS (WBC) S CASTS S CRYSTALS
S ABNORMAL EXCRETION OF SERUM PROTEIN (PROTEINURIA)
S REDUCTION IN GLOMERULAR FILTRATION RATE (AZOTEMIA)
S PRESENCE OF HYPERTENSION AND / OR EXPANDED TOTAL BODY FLUID VOLUME (EDEMA)
S ELECTROLYTE ABNORMALITIES
S FEVER / PAIN
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CLINICAL MANIFESTATION S DISTURBANCES IN URINE VOLUME (OLIGURIA, ANURIA,
POLYURIA)
S ABNORMALITIES OF URINE SEDIMENT, SUCH AS : RED BLOOD CELLS (RBC), WHITE BLOOD CELLS
(WBC), CASTS, CRYSTALS
S ABNORMAL EXCRETION OF SERUM PROTEIN (PROTEINURIA)
S REDUCTION IN GLOMERULAR FILTRATION RATE (AZOTEMIA)
S PRESENCE OF HYPERTENSION AND / OR EXPANDED TOTAL BODY FLUID VOLUME (EDEMA)
S ELECTROLYTE ABNORMALITIES
S FEVER / PAIN
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CLINICAL MANIFESTATION
S DISTURBANCES IN URINE VOLUME (OLIGURIA, ANURIA, POLYURIA)
S ABNORMALITIES OF URINE SEDIMENT S RED BLOOD CELLS (RBC) S WHITE BLOOD CELLS (WBC) S CASTS S CRYSTALS
S ABNORMAL EXCRETION OF SERUM PROTEIN (PROTEINURIA)
S REDUCTION IN GLOMERULAR FILTRATION RATE (AZOTEMIA)
S PRESENCE OF HYPERTENSION AND / OR EXPANDED TOTAL BODY FLUID VOLUME (EDEMA)
S ELECTROLYTE ABNORMALITIES
S FEVER / PAIN
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AZOTEMIA S DEFINITION :
S ABNORMALLY HIGH LEVELS OF NITROGEN CONTAINING COMPOUNDS, SUCH AS : UREA, CREATININE, VARIOUS BODY WASTE COMPOUNDS, AND OTHER NITROGEN RICH COMPOUNDS IN THE BLOOD
S ASSESSMENT OF GFR : S S.CREA IS THE MOST WIDELY USED MARKER FOR GFR S RELATED DIRECTLY TO THE U.CREA EXCRETION AND
S RELATED INVERSELY TO THE SERUM CREATININE
S PURPOSE : DRUGS DOSE ADJUSTMENT
S FORMULA :
UCr / PCr TIME PERIOD : USUALLY 24 HOURS
EXPRESSED IN ML / MIN
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AZOTEMIA
S COMPLICATION : S DRUG TOXICITIES
S SUCH AS : DIGOXIN AND AMINOGLYCOSIDES S SIGNIFICANT RISE IN MORBIDITY AND
MORTALITY
S UREMIA ( GFR < 15 ML / MIN ) S DEVELOP AT SIGNIFICANTLY DIFFERENT
LEVELS OF SERUM CREATININE DEPENDING ON : S PATIENT SIZE, AGE, AND SEX, S UNDERLYING RENAL DISEASE S EXISTENCE OF CONCURRENT DISEASE S TRUE GFR VALUE
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AZOTEMIA
REDUCED GFR
RETENSION OF NITROGENOUS
WASTE PRODUCTS AZOTEMIA UREMIA
REDUCED RENAL PERFUSION,
INTRINSIC RENAL DISEASE, OR
POST RENAL PROCESSES
PATHOPHYSIOLOGY :
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AZOTEMIA
METHOD TO MEASURE GFR
1. UREA CLEARANCE : S SIGNIFICANTLY UNDERESTIMATED GFR
S DUE TO TUBULE UREA REABSORPTION
2. CREATININE : S DERIVED FROM MUSCLE METABOLISM OF CREATINE,
S IT’S A SMALL, FREELY FILTERED SOLUTE
S SIGNIFICANTLY OVERESTIMATED GFR S SERUM CREATININE INCREASE ACUTELY FROM DIETARY
INGESTION OF COOKED MEAT
S CAN BE SECRETED INTO THE PROXIMAL TUBULE THROUGH AN ORGANIC CATION PATHWAY, LEADING TO OVERESTIMATION OF THE GFR
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AZOTEMIA
3. INULIN CLEARANCE
S BY MEASURING RADIONUCLIDE LABELED MARKERS SUCH AS 125I-IOTHALAMATE OR EDTA
S HIGHLY ACCURATE
S DUE TO PRECISE QUANTITATION AND THE ABSENCE OF ANY RENAL REABSORPTION / SECRETION
S USED TO FOLLOW GFR IN PATIENTS IN WHOM CREATININE IS NOT LIKELY TO BE A RELIABLE INDICATOR
S PATIENTS WITH DECREASED MUSCLE MASS SECONDARY TO AGE, MALNUTRITION, CONCURRENT ILLNESSES
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AZOTEMIA
4. CYSTATIN C S MEMBER OF THE CYSTATIN SUPERFAMILY OF
CYSTEINE PROTEASE INHIBITORS
S PRODUCED AT A RELATIVELY CONSTANT RATE FROM ALL NUCLEATED CELLS
S NOT AFFECTED BY DIET OR NUTRITIONAL STATUS
S MORE SENSITIVE INDICATOR OF GFR THAN THE PLASMA CREATININE CONCENTRATION
S REMAINS TO BE VALIDATED IN MANY CLINICAL SETTINGS
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AZOTEMIA
S FORMULA : S COCKCROFT – GAULT
S BASED ON AGE AND MUSCLE MASS
S THE VALUE SHOULD BE MULTIPLIED BY 0.85 FOR WOMEN DUE TO A LOWER FRACTION OF THE BODY WEIGHT & MUSCLE
S MDRD EQUATION
S MORE ACCURATE, BUT CUMBERSOME
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APPROACH TO THE PATIENT
• CLINICAL SITUATION & HISTORY
• LABORATORY DATA • ANEMIA, HYPOCALCEMIA, HYPERPHOSPHATEMIA
• CHARACTERISTIC OF CHRONIC RENAL FAILURE
• OFTEN ALSO PRESENT IN PATIENTS WITH ACUTE RENAL FAILURE
• URINALYSIS :
• PROTEINURIA, NON CONCENTRATED URINE (ISOSTHENURIA, ISOOSMOTIC WITH PLASMA)
• IMAGING TECHNIQUE • RENAL OSTEODYSTRIPHY (LATE FINDINGS)
• ULTRASOUND
• SMALL KIDNEYS
• INCREASED ECHOGENICITY AND CORTICAL THINNING
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APPROACH TO THE PATIENT
S DECREASED GFR :
S CLASSIFICATION (BASED ON DURATION) :
S ACUTE RENAL INJURY
S CHRONIC RENAL INJURY
S CLASSIFICATION (BASED ON ANATOMICAL ABNORMALITIES) :
S PRERENAL AZOTEMIA
S AFFECTING RENAL BLOOD FLOW
S INTRINSIC RENAL DISEASE
S AFFECTING SMALL VESSELS, GLOMERULI, OR TUBULES
S POSTRENAL PROCESSES
S OBSTRUCTION TO URINE FLOW IN URETERS, BLADDER, OR URETHRA
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APPROACH TO THE PATIENT
PRERENAL FAILURE
S DECREASE RENAL PERFUSION
S 40 – 80 % OF ACUTE RENAL FAILURE
S IF APPROPRIATELY TREATED – REVERSIBLE
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APPROACH TO THE PATIENT
PRERENAL FAILURE
S ETIOLOGY : S DECREASED CIRCULATING BLOOD VOLUME
S GI HEMORRHAGE, BURNS, DIARRHEA, DIURETICS
S VOLUME SEQUESTRATION
S PANCREATITIS, PERITONITIS, RHABDOMYOLISIS
S DECREASED EFFECTIVE ARTERIAL VOLUME
S CARDIOGENIC SHOCK, SEPSIS
S REDUCTION IN CARDIAC OUTPUT FROM PERIPHERAL VASODILATATION (SUCH AS : SEPSIS, DRUGS)
S PROFOUND RENAL VASOCONTRICTION
S SEVERE HEART FAILURE, HEPATORENAL SYNDROME, DRUGS, SUCH AS NSAIDS
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APPROACH TO THE PATIENT
PRERENAL FAILURE
S PATHOPHYSIOLOGY : S TRUE OR EFFECTIVE ARTERIAL HYPOVOLEMIA S FALL IN MEAN ARTERIAL PRESSURE S TRIGGERS A SERIES OF NEURAL AND HUMORAL
RESPONSES S ACTIVATION OF THE SYMPATHETIC NERVOUS, RAAS,
AND ADH RELEASE S COMPENSATORY MECHANISM (GFR IS MAINTAINED)
S PROSTAGLANDIN MEDIATED RELAXATION OF AFFERENT ARTERIOLES AND
S ANGIOTENSIN II MEDIATED CONSTRICTION OF EFFERENT ARTERIOLES
S DECOMPENSATED S STEEP DECLINE IN GFR, ONCE THE MEAN ARTERIAL
PRESSURE FALLS BELOW 80 MMHG
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APPROACH TO THE PATIENT
PRERENAL FAILURE
S PATHOPHYSIOLOGY : S TRUE OR EFFECTIVE ARTERIAL HYPOVOLEMIA S FALL IN MEAN ARTERIAL PRESSURE S TRIGGERS A SERIES OF NEURAL AND HUMORAL
RESPONSES S ACTIVATION OF THE SYMPATHETIC NERVOUS, RAAS,
AND ADH RELEASE S COMPENSATORY MECHANISM (GFR IS MAINTAINED)
S PROSTAGLANDIN MEDIATED RELAXATION OF AFFERENT ARTERIOLES AND
S ANGIOTENSIN II MEDIATED CONSTRICTION OF EFFERENT ARTERIOLES
S DECOMPENSATED S STEEP DECLINE IN GFR, ONCE THE MEAN ARTERIAL
PRESSURE FALLS BELOW 80 MMHG
NSAIDS – BLOCKADE OF PROSTAGLANDIN
ACE INHIBITORS
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APPROACH TO THE PATIENT
POSTRENAL FAILURE
S < 5 % OF CASES OF ACUTE RENAL FAILURE
S REVERSIBLE
S LOCATION : S OBSTRUCTION AT THE LEVEL OF URETHRA OR
BLADDER OUTLET S BILATERAL URETERAL OBSTRUCTION S UNILATERAL OBSTRUCTION IN PATIENT WITH A
SINGLE FUNCTIONING KIDNEY
S DIAGNOSIS : S PRESENCE OF URETERAL AND RENAL PELVIC
DILATATION ON RENAL ULTRASOUND
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APPROACH TO THE PATIENT
INTRINSIC RENAL DISEASE
S RULE OUT PRERENAL AND POSTRENAL
S ARISE FROM PROCESSES INVOLVING : S LARGE RENAL VESSELS,
S INTRARENAL MICROVASCULATURE AND GLOMERULI, OR
S TUBULOINTERSTITIUM
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APPROACH TO THE PATIENT
INTRINSIC RENAL FAILURE
S ISCHEMIC AND TOXIC ACUTE TUBULAR NECROSIS S 90 % OF ACUTE INTRINSIC RENAL FAILURE S MAJOR SURGERY, TRAUMA, SEVERE HYPOVOLEMIA,
OVERWHELMING SEPSIS, OR EXTENSIVE BURNS
S NEPHROTOXIC ACUTE TUBULAR NECROSIS S INDUCING A COMBINATION OF INTRARENAL
VASOCONTRICTION, DIRECT TUBULE TOXICITY, AND / OR TUBULE OBSTRUCTION
S KIDNEY IS VULNERABLE TO TOXIC INJURY S DUE TO ITS RICH BLOOD SUPPLY (25 % OF CARDIAC OUTPUT) AND
ITS ABILITY TO CONCENTRATE AND METABOLIZE TOXINS
S MANAGEMENT : S DISCONTINUATION OF NEPHROTOXINS AND STABILIZING BLOOD
PRESSURE
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APPROACH TO THE PATIENT
S DRUG INDUCED INTERSTITIAL NEPHRITIS S ETIOLOGY :
S ANTIBIOTICS, NSAIDS, AND DIURETICS, SEVERE INFECTIONS (BOTH BACTERIAL AND VIRAL), SYSTEMIC DISEASE (SYSTEMIC LUPUS ERYTHEMATOSUS), OR INFILTRATIVE DISORDERS (SARCOID, LYMPHOMA, OR LEUKEMIA)
S URINALYSIS
S MILD TO MODERATE PROTEINURIA, RBC, AND PYURIA (75 % OF CASES) AND OCCASIONALLY WBC CASTS
S RBC CASTS (CONSIDER GLOMERULAR DISEASES)
S EOSINOPHILS (SUGGESTIVE OF ALLERGIC INTERSTITIAL NEPHRITIS OR ATHEROEMBOLIC RENAL DISEASE),
S RENAL BIOPSY - TO DISTINGUISH AMONG INTERSTITIAL NEPHRITIS AND GLOMERULAR DISEASES
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APPROACH TO THE PATIENT
OCCLUSION OF LARGE RENAL VESSELS – ARTERIES AND VEINS
S AN UNCOMMON CAUSE OF ACUTE RENAL FAILURE S SUGGEST BILATERAL PROCESSES OR S A UNILATERAL PROCESS IN A PATIENT WITH
A SINGLE FUNCTIONING KIDNEY
S ETIOLOGY : S ATHEROEMBOLI, THROMBOEMBOLI, IN SITU
THROMBOSIS, AORTIC DISSECTION, OR VASCULITIS
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APPROACH TO THE PATIENT
OCCLUSION OF LARGE RENAL VESSELS – ARTERIES AND VEINS
S DIAGNOSIS :
S URINALYSIS :
S NORMAL URINALYSIS,
S (+) EOSINOPHILS AND CASTS – OCCASIONALLY
RENAL ARTERY THROMBOSIS MILD PROTEINURIA AND HEMATURIA
RENAL VEIN THROMBOSIS HEAVY PROTEINURIA AND HEMATURIA
DIAGNOSIS : REQUIRE ANGIOGRAPHY FOR CONFIRMATION
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APPROACH TO THE PATIENT
OLIGURIA S OLIGURIA - REFERS TO A 24 HOURS URINE
OUTPUT OF < 500 ML S ACCOMPANY ANY CAUSE OF ACUTE RENAL
FAILURE
S CARRIES A MORE SERIOUS PROGNOSIS FOR RENAL RECOVERY IN ALL CONDITIONS EXCEPT PRERENAL AZOTEMIA
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APPROACH TO THE PATIENT
ANURIA S REFERS TO THE COMPLETE ABSENCE OF
URINE FORMATION ( < 50 ML )
S ETIOLOGY : S TOTAL URINARY OBSTRUCTION
S TOTAL RENAL ARTERY OR VEIN OCCLUSION
S SHOCK (SEVERE HYPOTENSION AND INTENSE RENAL VASOCONSTRICTION)
S CORTICAL NECROSIS, ACUTE TUBULAR NECROSIS, AND RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS – OCCASIONALLY CAUSE ANURIA
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APPROACH TO THE PATIENT
NON OLIGURIA S URINE OUTPUT > 500 ML / DAY IN
PATIENTS WITH ACUTE OR CHRONIC AZOTEMIA
S LESS SEVERE DISTURBANCES OF POTASSIUM AND HYDROGEN BALANCE
S RECOVERY TO NORMAL RENAL FUNCTION IS USUALLY MORE RAPID
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APPROACH TO THE PATIENT
S TREATMENT : S SLOWING THE PROGRESSION OF RENAL
DISEASE AND
S PROVIDING SYMPTOMATIC RELIEF, FOR :
S EDEMA, ACIDOSIS, ANEMIA, AND HYPERPHOSPHATEMIA
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ABNORMALITIES OF THE URINE
S PROTEINURIA S PRESENCE OF AN EXCESS PROTEINS IN THE
URINE
S HEMATURIA S PRESENCE OF RED BLOOD CELLS
(ERYTHROCYTES) IN THE URINE
S PYURIA S URINE WHICH CONTAIN PUS
S CASTS S CYLINDRICAL STRUCTURES PRODUCED BY THE
KIDNEY AND PRESENT IN THE URINE IN CERTAIN DISEASE STATES
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ABNORMALITIES OF THE URINE
PROTEINURIA
S DIAGNOSIS : S DIPSTICK – DETECTS MOSTLY ALBUMIN
S DISADVANTAGE :
S FALSE POSITIVE RESULTS WHEN : S PH > 7.0 &
S THE URINE IS VERY CONCENTRATED OR CONTAMINATED
S OBSCURE SIGNIFICANT PROTEINURIA IN A VERY DILUTED URINE
S ULTRASENSITIVE DIPSTICK S TO MEASURE MICROALBUMINURIA 30 – 300 MG / DAY
S EARLY MARKER OF GLOMERULAR DISEASE, TO PREDICT GLOMERULAR INJURY IN EARLY DIABETIC NEPHROPATHY
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ABNORMALITIES OF THE URINE
PROTEINURIA
S PATHOPHYSIOLOGY :
S NORMAL :
S CHARGE AND SIZE SELECTIVITY OF THE GLOMERULAR WALL PREVENT VIRTUALLY ALL PLASMA ALBUMIN, GLOBULIN, AND OTHER LARGE MOLECULAR WEIGHT PROTEIN
S SMALLER PROTEIN ( < 20 kDA) ARE FREELY FILTRATED BUT ARE READILY REABSORBED BY THE PROXIMAL TUBULE
S NORMAL RANGE :
S < 150 MG / DAY OF TOTAL PROTEIN, OR
S < 30 MG / DAY OF ALBUMIN
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ABNORMALITIES OF THE URINE
PROTEINURIA S ABNORMAL :
S DISTRUPTED BARRIERS S LEAKAGE OF PLASMA PROTEINS INTO THE
URINE (GLOMERULAR PROTEINURIA) S EXCESSIVE PRODUCTION OF PROTEIN
S EXCEED THE CAPACITY OF THE TUBULE FOR REABSORPTION
S SUCH AS : S PLASMA CELL DYSCRASIAS (MM),
AMYLOIDOSIS, AND S LYMPHOMA THAT ARE ASSOCIATED WITH
MONOCLONAL PRODUCTION OF IMMUNOGLOBULIN LIGHT CHAINS
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ABNORMALITIES OF THE URINE
PROTEINURIA S ABNORMAL :
S DISTRUPTED BARRIERS S LEAKAGE OF PLASMA PROTEINS INTO THE
URINE (GLOMERULAR PROTEINURIA) S EXCESSIVE PRODUCTION OF PROTEIN
S EXCEED THE CAPACITY OF THE TUBULE FOR REABSORPTION
S SUCH AS : S PLASMA CELL DYSCRASIAS (MM),
AMYLOIDOSIS, AND S LYMPHOMA THAT ARE ASSOCIATED WITH
MONOCLONAL PRODUCTION OF IMMUNOGLOBULIN LIGHT CHAINS
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ABNORMALITIES OF THE URINE
PROTEINURIA S GLOMERULAR BASEMENT MEMBRANE
S GLOMERULAR ENDOTHELIAL CELL S PORES – 100 NM S OFFER LITTLE IMPEDIMENT
S GLOMERULAR BASEMENT MEMBRANE (GBM) S TRAPS MOST LARGE PROTEINS (> 100 KDA)
S PODOCYTES (FOOT PROCESSES) S SLIT DIAPHRAGMA S ALLOW WATER AND SMALL SOLUTES, BUT
NOT PROTEINS
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ABNORMALITIES OF THE URINE
PROTEINURIA S GLOMERULAR BASEMENT MEMBRANE
S GLOMERULAR ENDOTHELIAL CELL S PORES – 100 NM S OFFER LITTLE IMPEDIMENT
S GLOMERULAR BASEMENT MEMBRANE (GBM) S TRAPS MOST LARGE PROTEINS (> 100 KDA)
S PODOCYTES (FOOT PROCESSES) S SLIT DIAPHRAGMA S ALLOW WATER AND SMALL SOLUTES, BUT
NOT PROTEINS
MINIMAL CHANGES DISEASE FUSION OF FOOT PROCESSES – LARGER PORE SIZES – SELECTIVE LOSS OF ALBUMIN
IMMUNE COMPLEX DEPOSITION LOSS OF ALBUMIN AND OTHER PLASMA PROTEINS
IMMUNE COMPLEX DEPOSITION
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URINE PROTEIN ELECTROPHORESIS
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URINE PROTEIN ELECTROPHORESIS
EVALUATION OF PROTEINURIA
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ABNORMALITIES OF THE URINE
HEMATURIA
S NORMAL : S 2 MILLION OF RBC PER DAY
S HEMATURIA : S FEMALE : 2 – 5 RBCS PER HPF AND CAN BE DETECTED BY
DIPSTICK S MALE : 0 – 2 RBCS PER HPF AND CAN BE DETECTED BY
DIPSTICK
S SINGLE URINALYSIS WITH HEMATURIA (COMMON) S ETIOLOGY :
S MENSTRUATION, VIRAL ILLNESS, ALLERGY, EXERCISE, OR MILD TRAUMA
S PERSISTENT OR SIGNIFICANT HEMATURIA S > 3 RBCS / HPF ON THREE URINALYSIS, OR SINGLE URINALYSIS
WITH > 100 RBCS, OR GROSS HEMATURIA
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ABNORMALITIES OF THE URINE
HEMATURIA
S ISOLATED HEMATURIA S WITHOUT PROTEINURIA, OTHER CELLS, OR CASTS S INDICATIVE OF BLEEDING FROM THE URINARY
TRACT S COMMON CAUSES :
S STONES, NEOPLASMS, TUBERCULOSIS, TRAUMA, AND PROSTATITIS
S GROSS HEMATURIA S NEVER INDICATIVE OF GLOMERULAR BLEEDING S COMMON CAUSE :
S POST RENAL SOURCE IN THE URINARY COLLECTING SYSTEM
S ACUTE CYSTITIS OR URETHRITIS IN WOMEN
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ABNORMALITIES OF THE URINE
HEMATURIA, PYURIA, AND CASTS S HEMATURIA WITH PYURIA & BACTERIURIA
S TYPICAL OF INFECTION S SHOULD BE TREATED WITH ANTIBIOTICS AFTER
APPROPRIATE CULTURE
S ISOLATED MICROSCOPIC HEMATURIA S HYPERCALCIURIA AND HYPERURICOSURIA S MANIFESTATION OF GLOMERULAR DISEASE
S PHASE CONTRAST MICROSCOPY S DYSMORPHIC RBC
S MOST COMMON ETIOLOGY OF ISOLATED GLOMERULAR HEMATURIA S IGA NEPHROPATHY, HEREDITARY NEPHRITIS,
THIN BASEMENT MEMBRANE DISEASE
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ABNORMALITIES OF THE URINE
HEMATURIA, PYURIA, AND CASTS
S HEMATURIA WITH DYSMORPHIC RBCS, RBCS CASTS, AND PROTEIN EXCRETION OF > 500 MG / D S VIRTUALLY DIAGNOSTIC OF
GLOMERULONEPHRITIS S PATHOPHYSIOLOGY :
S RBC CASTS FORM AS RBCS THAT ENTER THE TUBULE FLUID BECOME TRAPPED IN A CYLINDRICAL MOLD OF GELLED TAMM-HORSFALL PROTEIN.
S EVEN IN THE ABSENCE OF AZOTEMIA, THESE PATIENTS SHOULD UNDERGO SEROLOGIC EVALUATION AND RENAL BIOPSY
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ABNORMALITIES OF THE URINE
HEMATURIA, PYURIA, AND CASTS
S ISOLATED PYURIA S UNUSUAL S INFLAMMATORY REACTION IN THE KIDNEY OFTEN
ACCOMPANIED WITH HEMATURIA
S BACTERIURIA, WITH WBC CASTS S INDICATIVE OF PYELONEPHRITIS
S WBC, AND / OR WBC CASTS S SEEN IN TUBULOINTERSTITIAL PROCESSES, SUCH AS
IN : S INTERSTITIAL NEPHRITIS, SYSTEMIC LUPUS
ERYTHEMATOSUS, AND TRANSPLANT REJECTION
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PYURIA
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ABNORMALITIES OF THE URINE
HEMATURIA, PYURIA, AND CASTS
S DEGENERATIVE CELLULAR CASTS (WAXY CASTS) S SEEN IN CHRONIC RENAL DISEASES
S BROAD CASTS S THOUGHT TO ARISE IN THE DILATED TUBULES OF
ENLARGED NEPHRONS THAT HAVE UNDERGONE COMPENSATORY HYPERTROPHY IN RESPONSE TO REDUCED RENAL MASS
S SUCH AS IN : CHRONIC RENAL FAILURE
S MIXTURE OF BROAD CASTS WITH CELLULAR CASTS AND RED BLOOD CELLS S SEEN IN SMOLDERING PROCESSES SUCH AS CHRONIC
GLOMERULONEPHRITIS
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RENAL BIOPSY
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(-)
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HYALINE CAST LEUKOCYTE CAST
ERYTHROCYTE CAST GRANULAR CAST
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ABNORMALITIES OF URINE VOLUME
S FACTORS CONTRIBUTING TO THE VOLUME OF URINE S FLUID INTAKE, RENAL FUNCTION, AND S PHYSIOLOGIC DEMANDS OF THE INDIVIDUAL
S CLASSIFICATION : S ANURIA
S ABSENCE OF URINE FORMATION, OR S URINE < 50 ML IN 24 HOURS
S OLIGURIA S URINE OUTPUT OF < 500 ML IN 24 HOURS
S POLYURIA S ABNORMALLY LARGE PRODUCTION AND / OR
PASSAGE OF URINE S URINE OUTPUT OF > 3 LITERS IN 24 HOURS
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ABNORMALITIES OF URINE VOLUME
S FACTORS CONTRIBUTING TO THE VOLUME OF URINE S FLUID INTAKE, RENAL FUNCTION, AND S PHYSIOLOGIC DEMANDS OF THE INDIVIDUAL
S CLASSIFICATION : S ANURIA
S ABSENCE OF URINE FORMATION, OR S URINE < 50 ML IN 24 HOURS
S OLIGURIA S URINE OUTPUT OF < 500 ML IN 24 HOURS
S POLYURIA S ABNORMALLY LARGE PRODUCTION AND / OR
PASSAGE OF URINE S URINE OUTPUT OF > 3 LITERS IN 24 HOURS
DISCUSSED PREVIOUSLY
DISCUSSED PREVIOUSLY
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ABNORMALITIES OF URINE VOLUME
S POLYURIA S > 3 LITERS / DAY S 2 POTENTIAL MECHANISM :
S EXCRETION OF NONABSORBABLE SOLUTES (GLUCOSE), OR
S EXCRETION OF WATER (DEFECT IN ADH PRODUCTION OR RENAL RESPONSIVENESS)
S DIAGNOSIS : S 24 HOURS URINE COLLECTION S URINE OSMOLALITY
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ABNORMALITIES OF URINE VOLUME
S URINE OSMOLALITY S NORMAL : 600 – 800 MOSM OF SOLUTES / DAY
S PRIMARILY AS UREA AND ELECTROLYTES
S WATER DIURESIS : S < 250 MOSM OF SOLUTES / LITER OF URINE
S < THAN 750 MOSM OF SOLUTES / DAY S ETIOLOGY :
S POLYDIPSIA, S INADEQUATE SECRETION OF VASOPRESSIN (CENTRAL
DIABETES INSIPIDUS), OR S FAILURE OF RENAL TUBULES TO RESPOND TO
VASOPRESSIN (NEPHROGENIC DIABETES INSIPIDUS)
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S SOLUTE DIURESIS : S > 300 MOSM OF SOLUTES / LITER OF URINE
S MORE THAN 900 MOSM OF SOLUTES / DAY
S SEARCH FOR RESPONSIBLE SOLUTE IS MANDATORY S GLUCOSE, MANNITOL, OR UREA
S ETIOLOGY : S DEPRESS REABSORPTION OF NACL AND WATER IN THE
PROXIMAL TUBULE
S POORLY CONTROLLED DIABETES MELLITUS WITH GLUCOSURIA (MOST COMMON)
S IATROGENIC
S SALT WASTING DISORDER
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S IATROGENIC SOLUTE DIURESIS S SUCH AS :
S MANNITOL ADMINISTRATION,
S RADIOCONTRAST MEDIA,
S HIGH PROTEIN FEEDINGS (ENTERALLY OR PARENTERALLY)
S PATHOPHYSIOLOGY :
S INCREASED UREA PRODUCTION AND EXCRETION
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ABNORMALITIES OF URINE VOLUME
S SALT WASTING DISORDERS : S ETIOLOGY :
S CYSTIC RENAL DISEASE – EXCESSIVE NA LOSS S BARTTER’S SYNDROME S TUBULOINTERSTITIAL PROCESS (RESOLVING
ATN) S PATHOPHYSIOLOGY :
S DIRECT IMPAIRMENT OF NA REABSORPTION, AND
S INDIRECT DECREASE OF THE TUBULE RESPONSIVENESS TO ALDOSTERONE
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