introduction to renal failure and acute renal failure jeffrey t. reisert, do university of new...
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Introduction to Renal Failure Introduction to Renal Failure and Acute Renal Failureand Acute Renal Failure
Jeffrey T. Reisert, DO
University of New England
Physician Assistant Program
20-27 JAN 20010
Contact InformationContact Information
Jeffrey T. Reisert, DO
103 Boulder Point Rd., Suite 3
Plymouth, NH 03264
603-536-6355
603-536-6356 (fax)
Genitourinary Section-Part 1Genitourinary Section-Part 1
Male urogenital disorders/Impotence Nephrolithiasis Urinary Tract Infections
Genitourinary Section-Part 2Genitourinary Section-Part 2
Introduction to Renal Failure Acute Renal Failure Chronic Renal Failure Glomerulopathies (builds on prior topics) Tubular disorders (builds on prior topics) Hematuria Proteinuria
Introduction Introduction
Two syndromes of renal failure– Acute– Chronic
Diagnosis-2 Patterns– Clinical suspect with signs and symptoms– Found incidentally on lab screen (serum or
urine)
AgendaAgenda
General evaluation of renal failure
– Definitions Acute Renal Failure (ARF)
– Etiology
– Diagnosis/Evaluation
– Treatment Chronic Renal Failure (CRF)
– Pathogenesis
– Complications
– Treatment of the complications
Definition-Renal failureDefinition-Renal failure
Spectrum of disease with declining kidney function
Decreased glomerular filtration rate Resultant increase in nitrogenous waste
products in the blood (azotemia) Alteration in fluid an electrolytes
Definitions-Part IIDefinitions-Part II
Oliguria=Urine output (UOP) of less than 400 or 500 cc/24 hours
Anuria=No UOP Uremia
– Decreased renal function– Azotemia– Symptoms
Definitions-Part IIIDefinitions-Part III Polyuria
– Excessive or frequent urination– Excessive water intake– Medical conditions?
Diabetes insipidus (Inability to concentrate urine)
– Renal disease Hematuria-blood in urine Proteinuria-protein in urine
AssessmentAssessment
Labs– Urine– Serum
Radiographic
Assessment-Labs IAssessment-Labs I
Blood urea nitrogen-BUN Creatinine BUN/Creatinine ratio
– >40 in prerenal azotemia– <20 in intrinsic renal failure
Electrolytes– Potassium especially!
CreatinineCreatinine
Goes up quickly in ARF due to ischemia and radio contrast (complication of x-ray dye studies such as IVP, CT scans)– Peaks 3-5d after contrast– Peaks 7-10d after ischemia
Not correlative with symptoms
ElectrolytesElectrolytes
Sodium reflects volume status Potassium, phosphate, and uric acid
increase
Assessment-Labs IIAssessment-Labs II
Urine output (UOP)-Monitor I’s and O’s Urine sodium (reflects concentrating ability
of kidneys) Body weight Toxin levels (i.e.: CPK-MM fraction in
rhabdomyolysis)
Glomerular filtration rateGlomerular filtration rate
Collectively, the measure of renal function– If low, leads to azotemia– Can be estimated by serum creatinine– Affected by age, sex, weight, fluid status, and
medical condition (illnesses, nutritional status, drugs on board, etc.)
– Creatinine used as a surrogate marker as levels vary little day-to-day.
Creatinine is secreted in the proximal tubule
Assessment-Labs IIIAssessment-Labs III
Creatinine clearance– ml/min/1.73 per square meter– Reflects the glomerular filtration rate– Normal 85-125– Lower in premies– Measured or Calculated methods (next slides)
Creatinine ClearanceCreatinine Clearance
[(Urine volume (ml/min) x Urine Creatinine)Divided by Serum Creatinine] x1.73/Body Surface Area
-Involves 24 hour urine test mated with serum creatinine-Fairly accurate and easy-Once a year?
Can be measured accurately by inulin (Usually in research)…..Is filtered but not reabsorbed or secreted in the renal tubules.
Also by radionuclide markers such as I125 iothalamate or EDTA (uncommon use) because……
Creatinine Clearance EstimatesCreatinine Clearance Estimates
Cockcroft-Gault equation Men:(140-age) x (wt in kg) divided by 72 x
serum creatine For women multiply by 85% to account for
smaller muscle mass (0.85 of men’s estimate)
Use in hospitals with IV antibiotic dosing
Assessment-Labs IIIAssessment-Labs III
Fractional excretion of Na+– (Urinary Na+ x Plasma Creatinine x 100%)
divided by (Plasma Na+ x Urinary Creatinine)
AzotemiaAzotemia
Defined as excess of urea and nitrogenous compounds in blood
Due to breakdown of protein (Metabolism of carbohydrates and fats
yields water and CO2) If symptoms, use term “uremia”
Assessment-RadiographicAssessment-Radiographic
Ultrasound– Excludes obstruction– ?Small kidneys--->CRF– Advantages
Non invasive No risky contrast dye Readily available
Assessment-Radiographic IIAssessment-Radiographic II
Plain x-Ray– Flat plate (?stone)
– Pyelogram-Inject a dye, cleared through kidney
– Retrograde pyelogram-Inject dye inside urinary collection system (intravesicular, using cystoscope)
CT– Probably better but dye risk in face of rising creatinine
MRI
Assessment-Wrap upAssessment-Wrap up
Avoid contrast in ARF or CRF not on dialysis
Biopsy may be needed in ARF for intrinsic disease
Ultrasound is easy and helpful
Complications of ARFComplications of ARF
Volume overload– Decreased sodium and water excretion– Resultant weight gain, heart failure, and edema
Hyponatremia Hypocalcemia
– Paresthesias, cramps, seizures, confusion
Complications of ARF IIComplications of ARF II
Hyperkalemia, phosphatemia, magnesemia– Potassium increases 0.5mmol/l/d in uremia– Treat hyperphosphatemia with calcium or
aluminum Metabolic acidosis Hypertension (Moreso in CRF)
General treatment of ARFGeneral treatment of ARF Prevention!!! (Avoid nephrotoxins, diabetes control,
etc.) Reverse poisons (ETOH in ethylene glycol,
bicarbonate in acidosis) Restore fluid volume and electrolyte balance
(Saline/crystalloids, colloids, blood) Dialysis when needed (Acute if responsive (i.e.:
dialyzable toxin) or in CRF) Relieve obstruction (Easiest way to fix ARF!)
Acute renal failureAcute renal failure
Definitions Classifications/Types Treatment
DefinedDefined
Renal failure of recent onset (hours to days to weeks)
Typically little symptoms– Can be found on random lab test or when
suspect– If acute obstruction, symptoms (below)
ClassificationClassification
Prerenal renal failure (Renal hypoperfusion)-55%
Renal/Parenchymal/Intrinsic-45% Post renal (Obstructive)-5%
OutcomeOutcome
Usually reversible Can recover even if almost no function Nephrology opinion?
Prerenal azotemiaPrerenal azotemia
Due to renal hypoperfusion Usually reversible if restoring renal blood
flow (RBF) Parenchyma usually not damaged In severe cases, ischemia/injury
EtiologyEtiology
Hypovolemia– Fluid loss– Decreased cardiac output– Decreased systemic vascular resistance
Renal hypoperfusion– See next slides
Fluid or blood lossFluid or blood loss
Dehydration GI bleeds Burns Osmotic diuresis (i.e.: diabetes) Sequestration (i.e.: pancreatitis)
Decreased Cardiac OutputDecreased Cardiac Output
Acute MI CHF (perhaps most common among
hospital patients) Arrhythmias Pulmonary embolism (PE) Mechanical ventilator
Altered systemic vascular Altered systemic vascular resistanceresistance
Sepsis, antihypertensives, anesthetics, anaphylaxis
HypovolemiaHypovolemia
Leads to epinephrine release and subsequent vasoconstriction
Also activations of renin angiotensin system-->Vasoconstriction
Release of arginine vasopressin (AVP)
Renal hypoperfusionRenal hypoperfusion
Renal vasoconstriction due to epinephrine ACE inhibitors Cyclooxygenase inhibitors (i.e.: NSAID’s)-
Also lead to volume depletion Hyperviscosity syndromes
Hepatorenal syndromeHepatorenal syndrome
Cirrhosis leads to intrarenal vasoconstriction
Sodium retention Precipitated by bleeding, paracentesis,
diuretics, vasodilation, cyclooxygenase inhibitors
Prerenal azotemia-Prerenal azotemia-AssessmentAssessment
Symptoms– Thirst, dizzy
Signs– Low blood pressure, tachycardia, orthostasis– Low UOP
Lab evaluationLab evaluation
Urine volume Urine microscopy
– Hyaline/bland casts due to concentrated urine
Intrinsic renal failureIntrinsic renal failure
Renovascular obstruction-Large vessel disease
Glomerular or microvascular diseases
Renovascular obstructionRenovascular obstruction
Obstructed renal artery (Atherosclerosis, thrombus)
Renal vein obstruction (Thrombosis, external compression)
Glomerular diseasesGlomerular diseases
Glomerulonephritis Vasculitis Acute tubular necrosis Ischemic or nephrotoxic Interstitial nephritis Renal allograft rejection Will expand in later section
VasculitisVasculitis
Kidneys are one of several very vascular organs Hemolytic uremic syndrome Thrombotic thrombocytopenic purpura Disseminated intravascular coagulation Toxemia Accelerated HTN Lupus ?Include sickle cell disease
Acute tubular necrosisAcute tubular necrosis
Most susceptible area of the nephron to ischemia is the renal tubule
Ischemia from prerenal azotemia (Most common)– Prerenal azotemia is the most common cause of
intrinsic renal failure Toxin induced Often see casts (covered later)
IschemiaIschemia
Hypoperfusion Resultant injury or ischemia Cortical necrosis Either recover (tubules regenerate) or
develop irreversible failure
NephrotoxinsNephrotoxins
Radiocontrast (Intrarenal vasoconstriction) Aminoglycosides (Decrease GFR) Cyclosporin Chemotherapy (Cisplatin) Solvents (ethylene glycol) Others
Endogenous nephrotoxinsEndogenous nephrotoxins
Rhabdomyolysis (Due to crush, injury, ETOH)
Hemolysis (toxic to renal tubule) Uric acid (Same thing that causes gout) Myeloma (Plasma cell malignancy) Hypercalcemia (Causes renal
vasoconstriction)
Interstitial NephritisInterstitial Nephritis
Allergic (Antibiotics such as beta-lactams), NSAID’s, diuretics
Infection (Bacterial-pyelonephritis, viral-CMV, Fungus-Candidiasis)
Infiltration (Lymphoma, leukemia, sarcoidosis)
Idiopathic
Intrinsic renal failureIntrinsic renal failure
Symptoms-Often none May have history of nephrotoxin exposure Signs-Azotemia on lab testing Nephritic syndrome (Oliguria, edema,
HTN, Urine sediment)– This suggests a glomerulonephritis or vasculitis
Intrinsic renal failure-Lab Intrinsic renal failure-Lab evaluationevaluation
Microscopy– Muddy brown casts (ischemia and nephrotoxic)– Red cell casts (acute glomerular injury or
nephritis)– White cell casts (interstitial nephritis)– Eosinophilic casts (allergic nephritis)– Often no casts– Hematuria
Intrinsic renal failure-Lab Intrinsic renal failure-Lab evaluationevaluation
Proteinuria due to impaired reabsorption at the proximal tubules
Guided by etiology (i.e.: sedimentation rate if vasculitis)
Intrinsic renal failure-Intrinsic renal failure-TreatmentTreatment
Treat cause Remove insult Support, hope, and pray
ExamplesExamples
Glucocorticoids in vasculitis and allergic interstitial nephritis)
Control blood pressure
Postrenal renal failurePostrenal renal failure
Urinary outflow obstruction Single kidney or urethral obstruction--
>Anuria
Etiologies of postrenal Etiologies of postrenal azotemiaazotemia
Prostate disease Neurogenic bladder
– I.e.: spinal cord injuries Anticholinergics Blood clots Stones Tumor or other extrarenal obstruction
Postrenal signs and Postrenal signs and symptomssymptoms
Bladder distension Abdominal pain-colic Renal distension (ultrasound) History of risk factors (prostate disease,
stones, etc.)
Treatment of obstructionTreatment of obstruction
Urologist Fix plumbing May need nephrostomy tube or suprapubic
catheter placed
Miscellaneous treatment Miscellaneous treatment wrap-upwrap-up
Loop diuretics may restore diuresis Dopamine may promote sodium and water
excretion Dialysis when needed
Wrap-up II--Dialysis UseWrap-up II--Dialysis Use
?BUN > 100 Uremia Hypervolemia Hyperkalemia Acidosis Toxins
– Multiple
– Include digoxin, others
More……More……
…to come in next slide set