Professional Documents
Culture Documents
OF KIDNEY FUNCTIONS
Painless, non-invasive,
inexpensive.
FRESH SAMPLE!!
Urine samples
Gross appearance
Amount
– 800 – 1800 mL / die
– Polyuria > 2.5 L / die
– Oliguria < 400 mL / die, Anuria 100 ml / die
– Pollakisuria: frequent, but small amount, becasue of tumor or
infection
Color
– Normally yellowish
– Food, drugs
– Blood, myoglobin
Transparency
– Infection, blood, bacteria, fungi
Odor
typical urine smell
sweet: sugar
ammoniac
Biochemical Tests of Renal Function
pH
Glucose
Protein
Microalbuminuria
RBC
Haemoglobin
WBC
Nitrit
Bilirubin
Urobilinogen
Keton bodies
Specific gravity
Osmolality
Urine sediment: microscopic examination
from freshly passed urine
Microscopic analysis
should follow when the
biochemical tests are
positive.
Analyze spontaneous-urine
sample within 4 h after
sampling.
Clearance = (U x V) / P where
U = is the urinary concentration of a given substance
V = is the volume of urine produced (mL/min)
P = is the plasma concentration of the given substance
1-2 % / day of
muscle creatine
converted to
creatinine.
Amount produced
relates to muscle
mass.
Freely filtered at the
glomerulus.
Some tubular
excretion.
Creatinine Clearance
Timed urine collection for
creatinine measurement
(usually 24h)
Blood sample taken within the
period of collection.
In vitro interference:
Problems: acetoacetate, ascorbic acid,
Practical problems of accurate fructose, pyruvate,
urine collection and volume cephalosporins, creatine,
measurement. proline, chronic lidocaine
administration, bilirubin.
Within subject variability =
In vivo inhibition of
11%
creatinine secretion occurs
Interference in creatinine with cimetidine or
measurement trimethoprim.
Estimated GFR (eGFR)
Plasma Creatinine Concentration
Difficulties:
Concentration depends on balance between input
and output.
Production determined by muscle mass which is
related to age, sex and weight.
High between subject variability.
Concentration inversely related to GFR.
– Small changes in creatinine within and around the
reference limits = large changes in GFR.
Reference limits can be misleading.
Estimated GFR (eGFR)
Plasma Creatinine Concentration: Problems
Plasma creatinine can increase following protein
loads.
– Goulash effect: 80% rise in creatinine after 300g of
cooked beef.
– Less variability in early morning creatinine
Strenuous exercise may increase creatinine by 14%
Muscle mass more difficult to predict in oedematous
patients and late pregnancy
Patients with muscle wasting
Patients with liver disease
Drugs inhibiting tubular secretion can raise
creatinine concentration.
Effect of Muscle Mass on Serum Creatinine
Normal
Muscle
Mass
Creatinine
Input
Kidney output
Normal
Kidneys
Effect of Muscle Mass on Serum Creatinine
Normal Normal
Muscle Muscle
Mass Mass
Creatinine
Input
Creatinine
Plasma
Level
Kidney output
Normal Diseased
Kidneys Kidneys
Effect of Muscle Mass on Serum Creatinine
Increased
Normal Normal Muscle
Muscle Muscle Mass
Mass Mass
Creatinine
Input
Creatinine
Plasma
Level
Kidney output
Normal Diseased Normal
Kidneys Kidneys Kidneys
Effect of Muscle Mass on Serum Creatinine
Increased
Normal Normal Muscle
Reduced
Muscle Muscle Mass
Muscle
Mass Mass Mass
Creatinine
Input
Creatinine
Plasma
Level
Kidney output
Normal Diseased Normal Diseased
Kidneys Kidneys Kidneys Kidneys
Estimated GFR (eGFR)
Plasma Creatinine
Concentration: Problems
Cystatin-C
Cysteine proteinase Estimation of GFR for/in:
inhibitor C (MW13 000) – Early detection of kidney
Small size = freely filtered disease
at glomerulus – Acute and chronic renal
Constant production rate disease
by all nucleated cells – Renal transplantation and
No known extra-renal haemodialysis
excretion routes – Diseases associated with
Not influenced by muscle kidneys, e.g. diabetes
mass, diet or sex mellitus, hypertension
– Patients receiving
nephrotoxic drugs
– Liver failure
– Paediatrics and elderly
Guidelines for the estimation of GFR
in the clinical practice
– It is IRREVERSIBLE
Acute Renal Failure (ARF)
Sudden loss of kidney function over a
period of hours or days
– Characterized by:
A rapid ↓ GFR
Retention of metabolic waste
– A progressive ↑ BUN and ↑ Creatinine (Azotemia)
– Associated with:
Classic finding of Oliguria (UO < 400ml/day)
Fluid, electrolyte and acid-base imbalances
– Usually reversible with prompt treatment
Classification of ARF: according to the
location of the insult
– Prerenal
↓ Blood flow to kidneys
Occurs in about 50-70% of all
ARF cases
– Intrarenal
actual damage to kidneys
Occurs in about 20-30% of all
ARF cases
– Postrenal
obstruction of urinary excretion
Occurs in about 1-10% of all ARF
cases
Pre-Renal ARF
Renal blood flow is decreased before reaching
the kidney.
– ↓ Renal Perfusion = ↓ GFR leading to Oliguria
– Most common type of ARF
– Common Causes:
Hypotension (severe and abrupt)
Hypovolemia
Low Cardiac Output States
– Treatment to correct cause, if not corrected it may
cause intrarenal failure i.e. acute tubular necrosis
(ATN)
Intrarenal ARF: a condition that leads to actual
damage of the renal tissue (parenchyma) resulting
in malfunction of nephrons.
TEST RESULT
Pre-renal Renal
TEST RESULT
Pre-renal Renal
Urine / Plasma
Osmolality > 1.5 : 1 < 1.1 : 1
Urine urea cc /
Plasma urea cc > 10 < 5
Postrenal ARF: conditions that block
urine flow distal to kidneys
– Caused by an obstruction below
the kidneys in the urinary tract
Calculi (stones)
Tumors or masses
Blood clots
Benign prostate hypertrophy (BPH)
Vascular disorders
Infections
Nephrotoxic medications
Toxic agent exposure
Sickle cell anemia
Systemic lupus erythematosus
Pyelonephritis
Obstructions of the urinary tract
Polycystic kidney disease
Three Stages of CRF
Stage 1
– Reduced renal reserve Stage 3
Characterized by a 40-75% loss of – End-stage renal
nephron function disease (ESRD)
Usually asymptomatic; normal BUN Final Stage
& Creatinine
Characterized by
Stage 2 a >90% loss of
– Renal Insufficiency nephron function
Characterized by a 75-90% loss of Characterized by
nephron function ↑BUN ↑Creatinine
↑BUN and ↑Creatinine and electrolyte
– Kidneys loose ability to concentrate imbalances
urine; client may report polyuria
or/and nocturia; Anemia develops
Uremic
symptoms
Requires Life-
long Dialysis
Nephrotic syndrome
Pathophysiology of nephrotic syndrome
Increased glomerular
capillary permeability
Heavy proteinuria
Susceptibility Compensatory
Edema
to infection Increase in lipoprotein
synthesis
Hyperlipemia Hypercoagulability
Systemic biochemical manifestations,
complications
Anemia – Increased triglyceride
– Inadequate erythropoietin production levels
– Decreased life span of RBC Occurs in 30-70% in CFR
– Nutritional deficits – Increased blood sugars
S/SX: fatigue, shortness of breath Usually moderate; alterations
and even angina cellular use of glucose
Renal Osteodystrophy – Increased tendency to
– A syndrome of skeletal changes bleed
found in CRF from alterations in Altered platelet function and
calcium & phosphate metabolism and coagulation factors
elevated PTH levels: – Increased risk of Infection
↑ PTH reabsorbs calcium & Impaired leukocyte function
phosphorous from bone stores in an and immune responses
attempt to increase serum calcium
levels. – Reproductive Dysfunction
Long term effects: bone deformity Infertility and decreased libido
and weakness
Biochemical manifestations: electrolyte
imbalances
– Hyperkalemia
Kidney’s can’t excrete 80-90% of body’s potassium like normal
Irritability, restlessness, weakness, diarrhea and abdominal
pain/cramping
– Hyperphosphatemia
Primarily excreted by kidneys; ↓UO = decreased excretion
– Hypocalcemia
The active form of Vitamin D is required for Ca2+ to be absorbed;
only functioning kidneys can activate Vitamin D
– Hypermagnesemia
Usually normal or slightly elevated
– Hyponatremia
Sodium levels maybe decreased due to hemodilution from fluid
overload.
Thank you!