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

ALL ABOUT INTERNAL MEDICINE (AAIM)

S

AZOTEMIA AND URINARY ABNORMALITIES

HARRISON’S PRINCPLES OF INTERNAL MEDICINE 17TH EDITION

CHAPTER 45, PAGE 268 - 274


S ALL ABOUT INTERNAL MEDICINE (AAIM)



ANATOMY

RENAL CORPUSCLE

RENAL TUBULE & MEDULLARY RAYS COLLECTING

DUCT RENAL PAPILLA

MINOR & MINOR CALYCES

RENAL PELVIS

URETER



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



NEPHRONS

URINE PRODUCING FUNCTIONAL STRUCTURES OF THE KIDNEY



NEPHRONS

Efferent Arteriole

Afferent Arteriole

Juxtaglomerular Cell

Pedicel

Podocyte

Parietal Layer Of The Bowman’s Capsule

Proximal Convoluted Tubules

Capsular Space



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







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



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  FEVER / PAIN



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  FEVER / PAIN



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  FEVER / PAIN



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

REDUCED GFR

RETENSION OF NITROGENOUS

WASTE PRODUCTS AZOTEMIA UREMIA

REDUCED RENAL PERFUSION,

INTRINSIC RENAL DISEASE, OR

POST RENAL PROCESSES

PATHOPHYSIOLOGY :



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



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

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



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



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






PRERENAL FAILURE

S  DECREASE RENAL PERFUSION

S  40 – 80 % OF ACUTE RENAL FAILURE

S  IF APPROPRIATELY TREATED – REVERSIBLE




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)

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




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




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




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




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




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

S  LESS SEVERE DISTURBANCES OF POTASSIUM AND HYDROGEN BALANCE

S  RECOVERY TO NORMAL RENAL FUNCTION IS USUALLY MORE RAPID














S  TREATMENT : S  SLOWING THE PROGRESSION OF RENAL

DISEASE AND

S  PROVIDING SYMPTOMATIC RELIEF, FOR :

S  EDEMA, ACIDOSIS, ANEMIA, AND HYPERPHOSPHATEMIA



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

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






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 – 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





URINE PROTEIN ELECTROPHORESIS



URINE PROTEIN ELECTROPHORESIS

EVALUATION OF PROTEINURIA




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




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





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





RENAL BIOPSY



(-)









HYALINE CAST LEUKOCYTE CAST

ERYTHROCYTE CAST GRANULAR CAST



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 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




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  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  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



















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

Documents

immunoglobulin

fever pain

prostaglandin

systemic lupus

solutes liter

clinical manifestations

red blood

white blood