Azotemia &amp Urinary Abnormalities - Chapter 45 - All About Internal Medicine (AAIM)

AZOTEMIA AND URINARY ABNORMALITIES
HARRISONS PRINCPLES OF INTERNAL MEDICINE 17TH EDITION CHAPTER 45, PAGE 268 - 274
S
ALL ABOUT INTERNAL MEDICINE (AAIM)
S
ANATOMY
RENAL CORPUSCLE RENAL TUBULE & MEDULLARY RAYS RENAL PAPILLA MINOR & MINOR CALYCES RENAL PELVIS
COLLECTING DUCT
URETER
S
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
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
S
NEPHRONS
URINE PRODUCING FUNCTIONAL STRUCTURES OF THE KIDNEY
NEPHRONS
Afferent Arteriole Juxtaglomerular Cell Parietal Layer Of The Bowmans Capsule Capsular Space Efferent Arteriole Proximal Convoluted Tubules Podocyte Pedicel
S
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
S
S
S
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 S S
S S
(PROTEINURIA) REDUCTION IN GFR (AZOTEMIA) PRESENCE OF HYPERTENSION AND / OR EXPANDED TOTAL BODY FLUID VOLUME (EDEMA) ELECTROLYTE ABNORMALITIES FEVER / PAIN
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
S
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
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
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
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
AZOTEMIA
PATHOPHYSIOLOGY :
REDUCED RENAL PERFUSION, INTRINSIC RENAL DISEASE, OR POST RENAL PROCESSES

REDUCED GFR
RETENSION OF NITROGENOUS WASTE PRODUCTS
AZOTEMIA
UREMIA
S
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 ITS 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
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
AZOTEMIA
4. CYSTATIN C
S MEMBER OF THE CYSTATIN SUPERFAMILY OF S S S S
CYSTEINE PROTEASE INHIBITORS PRODUCED AT A RELATIVELY CONSTANT RATE FROM ALL NUCLEATED CELLS NOT AFFECTED BY DIET OR NUTRITIONAL STATUS MORE SENSITIVE INDICATOR OF GFR THAN THE PLASMA CREATININE CONCENTRATION REMAINS TO BE VALIDATED IN MANY CLINICAL SETTINGS
S
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
S
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

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
S

PRERENAL FAILURE
S DECREASE RENAL PERFUSION S 40 80 % OF ACUTE RENAL FAILURE S IF APPROPRIATELY TREATED REVERSIBLE
S

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

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)
PROSTAGLANDIN MEDIATED RELAXATION OF AFFERENT ARTERIOLES AND S ANGIOTENSIN II MEDIATED CONSTRICTION OF EFFERENT ARTERIOLES
S
S DECOMPENSATED S STEEP DECLINE IN GFR, ONCE THE MEAN ARTERIAL PRESSURE FALLS BELOW 80 MMHG

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 COMPENSATORYNSAIDS BLOCKADE OF PROSTAGLANDIN MECHANISM (GFR IS MAINTAINED)
PROSTAGLANDIN MEDIATED RELAXATION OF AFFERENT ARTERIOLES AND S ANGIOTENSIN II MEDIATED CONSTRICTION OF EFFERENT ARTERIOLES
S
S DECOMPENSATED S STEEP DECLINE IN GFR, ONCE THE MEAN ARTERIAL PRESSURE FALLS BELOW 80 MMHG
ACE INHIBITORS

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 PRESENCE OF URETERAL AND RENAL PELVIC
S DIAGNOSIS :
DILATATION ON RENAL ULTRASOUND

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
S

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

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

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

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
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
S
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
NON OLIGURIA
S URINE OUTPUT > 500 ML / DAY IN
PATIENTS WITH ACUTE OR CHRONIC AZOTEMIA POTASSIUM AND HYDROGEN BALANCE FUNCTION IS USUALLY MORE RAPID
S LESS SEVERE DISTURBANCES OF S RECOVERY TO NORMAL RENAL
S
S
S
S
S

S TREATMENT : S SLOWING THE PROGRESSION OF RENAL
DISEASE AND S PROVIDING SYMPTOMATIC RELIEF, FOR : S EDEMA, ACIDOSIS, ANEMIA, AND HYPERPHOSPHATEMIA
S
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

PROTEINURIA
S DIAGNOSIS : S DIPSTICK DETECTS MOSTLY ALBUMIN
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
S
S

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

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

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
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
PROTEINURIA
S GLOMERULAR BASEMENT MEMBRANE
S GLOMERULAR ENDOTHELIAL CELL S PORES IMMUNE COMPLEX DEPOSITION 100 NM S OFFER LOSS OF ALBUMIN AND OTHER PLASMA PROTEINS LITTLE IMPEDIMENT S GLOMERULAR BASEMENT MEMBRANE (GBM) S TRAPS MOST LARGE PROTEINS (> 100 KDA) IMMUNE COMPLEX DEPOSITION S PODOCYTES (FOOT PROCESSES) S SLIT DIAPHRAGMA MINIMAL CHANGES S ALLOW WATER ANDOF FOOT PROCESSES BUT FUSION SMALL SOLUTES,
ALBUMIN
DISEASE
NOT PROTEINS LARGER PORE SIZES SELECTIVE LOSS OF
S
URINE PROTEIN ELECTROPHORESIS
S
EVALUATION OF PROTEINURIA URINE PROTEIN ELECTROPHORESIS
S

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

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

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

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 TAMMHORSFALL PROTEIN. S EVEN IN THE ABSENCE OF AZOTEMIA, THESE PATIENTS SHOULD UNDERGO SEROLOGIC EVALUATION AND RENAL BIOPSY

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
PYURIA

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
S
S RENAL BIOPSY
(-)
S
S
S
S
HYALINE CAST
LEUKOCYTE CAST
ERYTHROCYTE CAST
GRANULAR CAST
S
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

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 DISCUSSED PREVIOUSLY 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
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

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)

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
S

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
S

S SALT WASTING DISORDERS : S ETIOLOGY : S CYSTIC RENAL DISEASE EXCESSIVE NA LOSS S BARTTERS SYNDROME S TUBULOINTERSTITIAL PROCESS (RESOLVING ATN) S PATHOPHYSIOLOGY : S DIRECT IMPAIRMENT OF NA REABSORPTION, AND S INDIRECT DECREASE OF THE TUBULE RESPONSIVENESS TO ALDOSTERONE
S
S
S
S
S
S
S
S
S

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AZOTEMIA AND URINARY ABNORMALITIES

ALL ABOUT INTERNAL MEDICINE (AAIM)

URINE PRODUCING FUNCTIONAL STRUCTURES OF THE KIDNEY

ALL ABOUT INTERNAL MEDICINE (AAIM)

S ABNORMALITIES OF URINE SEDIMENT

S ABNORMAL EXCRETION OF S. PROTEIN S S

ALL ABOUT INTERNAL MEDICINE (AAIM)

S REDUCTION IN GLOMERULAR FILTRATION

S PRESENCE OF HYPERTENSION AND / OR EXPANDED TOTAL BODY

FLUID VOLUME (EDEMA)

S ELECTROLYTE ABNORMALITIES S FEVER / PAIN

S ABNORMALITIES OF URINE SEDIMENT, SUCH AS :

S REDUCTION IN GLOMERULAR FILTRATION RATE

S PRESENCE OF HYPERTENSION AND / OR EXPANDED TOTAL

BODY FLUID VOLUME (EDEMA)

S ELECTROLYTE ABNORMALITIES S FEVER / PAIN

FLUID VOLUME (EDEMA)

S ELECTROLYTE ABNORMALITIES S FEVER / PAIN

S PURPOSE : DRUGS DOSE ADJUSTMENT S FORMULA :

ALL ABOUT INTERNAL MEDICINE (AAIM)

S UREMIA ( GFR < 15 ML / MIN )

ALL ABOUT INTERNAL MEDICINE (AAIM)

REDUCED RENAL PERFUSION, INTRINSIC RENAL DISEASE, OR POST RENAL PROCESSES

INGESTION OF COOKED MEAT

THROUGH AN ORGANIC CATION PATHWAY, LEADING TO OVERESTIMATION OF THE GFR

ALL ABOUT INTERNAL MEDICINE (AAIM)

ALL ABOUT INTERNAL MEDICINE (AAIM)

APPROACH TO THE PATIENT

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APPROACH TO THE PATIENT

ABNORMALITIES) : S PRERENAL AZOTEMIA

TUBULES S POSTRENAL PROCESSES

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VASODILATATION (SUCH AS : SEPSIS, DRUGS)

DRUGS, SUCH AS NSAIDS

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DILATATION ON RENAL ULTRASOUND

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AND GLOMERULI, OR S TUBULOINTERSTITIUM

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OVERWHELMING SEPSIS, OR EXTENSIVE BURNS

S MANAGEMENT : S DISCONTINUATION OF NEPHROTOXINS AND STABILIZING BLOOD PRESSURE

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(75 % OF CASES) AND OCCASIONALLY WBC CASTS

NEPHRITIS OR ATHEROEMBOLIC RENAL DISEASE),

NEPHRITIS AND GLOMERULAR DISEASES

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S ETIOLOGY : S ATHEROEMBOLI, THROMBOEMBOLI, IN SITU

THROMBOSIS, AORTIC DISSECTION, OR VASCULITIS

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