Flashcards in Alex: Chronic Kidney Disease (Epidemiology and Adaptations) Deck (48)
What are a the functions of he kidney
Elimination of Nitrogenous waste
Water and electrolyte balance
Endocrine activity (Vitamin D, erythropoietin, renin, prostaglandins
Produce vasoactive compounds (ie. prostaglandins, nitric oxide, angiotensin II, endothelin).
Define Chronic Kidney Disease (CKD)
Kidney damage for >3 months, as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifest by either :
1.Pathological abnormalities of the kidney
2.Markers of kidney damage, including abnormalities in the composition of the blood or urine or abnormal imaging tests of the kidneys
GFR 3 months, with or without markers of kidney damage
What are some examples of STRUCTURAL abnormalities seen in CKD ?
Multiple renal cysts
Presence of only one kidney
What are some examples of FUNCTIONAL abnormalities seen in CKD ?
Microalbuminuria (Diabetes, HTN, Obesity)
Proteinuria (Large amounts of protein)
How can you differentiate CKD from Acute Kidney Injury ?
AKI: Serum Creatinine > 0.3 mg/dl (days to weeks)
CKD: Decrease in GFR or signs of renal injury (>3 months duration)
The Cockcroft and Gault formula takes into account which variables when estimating GFR ?
Age and Weight
the MDRD Formula takes into account which variables when estimating GFR ?
Age, Sex and Weight.
Males typically have a ______ GFR than females. Why ?
Increased Muscles Mass
Younger patients typically have a _______GFR than older patients. Why
Increased Muscles Mass
African American patients typically have a ______ GFR than caucasians . Why ?
Increased Muscles Mass
Stage O Kidney disease
GFR > 90 with CKD risk Factors
Stage I Kidney disease
GFR >90 , Chronic Kidney damage with normal GFR
Stage II Kidney disease
GFR 60-89 , Mild GFR decrease
Stage III Kidney disease
GFR 30-59 , Moderate GFR Decrease
Stage IV KD
GFR 15-29, Severe GFR Decerase
Stage V KD
Kidney failure, GFR < 15 or Dialysis
List 6 risk factors for CKD
Ethnic (African Americans)
When does the rate of GFR typically begins to increase ?
As you age, around age 40.
The incidence of CKD is rising for all age groups but is most pronounced in which group ?
What stage of Kidney Disease is this patient in : A patient with autosomal dominant polycystic kidney disease with cysts in the kidneys by ultrasound and a GFR of 100 ml/min
Stage I (GFR is over 90 but there is evidence of chronic kidney damage)
What stage of Kidney Disease is this patient in: A patient with IgA nephropathy with increased echogenicity of the kidneys on ultrasound and a GFR of 70 ml/min
Stage II (GFR 60-89) with kidney damage.
What stage of Kidney Disease is this patient in : A patient with long-standing HTN, 8 cm kidneys by ultrasound (small) and a GFR of 32 ml/min
Stage III (GFR 30-59)
What are the 4 key issues in the management of CKD
1. Treat any reversible causes of renal dysfunction (ie. volume depletion, AKI)
2.Prevent or slow the progression of disease
3.Treat the complications of kidney failure
4.Prepare the patient for renal replacement therapy (ie. dialysis or transplantation)
The Initial Evaluation of CKD involves 7 Steps. List them
1.Obtain serum creatinine to calculate eGFR
2.Measure protein/creatinine ratio or albumin/creatinine ratio in first AM (morning) or random urine
3.Examine the urine sediment for RBCs, WBCs, and cellular casts
4.Imaging study of kidneys- Ultrasound (always!)
5.Serum electrolytes (Na, K, Cl, HCO3,) and chemistries (calcium, phosphorous)
7.Measure parathyroid hormone level (PTH)
One of the reversible factors leading to a reduction in kidney function is to dehydration. What can cause this ?
Decreased Fluid Intake
Increased Fluid Output (Use of diuretics, Diabetes Insipidus)
Including Dehydration, what are the 5 reversible factors that can lead to a reduction in kidney function ?
2. Accelerated HTN
3.Heart Failure with poor renal perfusion
4.Nephrotoxic substances (IV contrast, NSAIDs) DO NOT USE CONTRAST (if you can help it)
5.Urinary tract infection/obstruction
End Stage Renal Disease is also known as ...
Stage V CKD requiring Dialysis or Transplant
It the maintenance of the volume and composition of the ECF well conserved or impaired until late in the course of CKD ?
Surprisingly, it is well preserved
What occurs to allow for compensation in response to loss of functioning nephrons in CKD ?
Nephron hypertrophy and hyper function (combine to compensate for the loss of functioning nephrons)
THERE IS NO HYPERPLASIA ..no ability to create new nephrons.
Adaptive changes in the nephron may lead to ....
maladaptive long-term consequences
The effort of the kidney to correct a low GFR may eventually lead to progression of renal failure
In order for the remaining nephrons to compensate for the lost ones, what three things must be achieved by the available nephrons ? (Intact Nephron Hypothesis)
1.Increase its own GFR (Single nephron GFR) This process is called Compensatory Hyperfiltration....
2.Increase its own net acid (H+) secretion (ammonium generation- ammoniagenesis)
Limits metabolic acidosis
3.Increase its own sodium and water excretion
Where in the nephron will the adaptions needed to achieve increased sodium, H20 and ammonium excretion (Intact Nephron Hypothesis) occur ?
The Tubules (tubular hypertrophy)
Where in the nephron will the adaptions needed to achieve increased Urea excretion occur ?
At the glomerulus
Only an increase in the GFR of that single nephron will permit more BUN excretion
What occurs at the level of the glomerular capillaries to allow for increased sodium, H20 and ammonium excretion ?
Increased Vasodilation of the Afferent Arteriole
Increased Vasoconstriction of the Effertent Arteriole.
Overally this will lead to increased intraglomerular pressure and GFR
What molecules are responsible for increased Afferent Arteriole Vassodilation ?
Vasodilatory prostaglandins (PGE2 / PGI2)
What molecule is responsible for Efferent Arteriole Vasoconstriction ?
The overall effect of the Intact Nephron Hypothesis is maladaptive ......
Intaglomerular hypertrophy will lead to glomerular stretch/growth and hypertrophy. This will cause...
What occurs in nehphrons who undergo long term HTN and hypertrophy ?
Long term effect is to develop progressive scarring of the mesangium / glomerulus
Increases wall stress on the vessels and mesangium results in increased production of matrix and collagen to prevent overstretching of the glomerulus
due to Impaired renal ammonia genesis and Reduced filtration of titratable acids, what will occur in all CKD patients over time ?
Metabolic Acidosis !
Although increased ammoniagenesis is good for short term prevention of metabolic acidosis, what is the long term effect ?
Ammonia is highly inflammatory to the renal interstitium
Results in complement activation and Progressive deposition of collagen and matrix leading to interstitial fibrosis
Once renal adaptation to CKD (Intraglomerular HTN, Glomerular hypertrophy, increased ammonia genesis) is initiated can you halt progression by fixing the original disease ?
renal function continues to decline even if the original disease or cause of injury is not present any longer
With nephron loss, what molecule will be increased to help the tubules deal with an increased Na+(fluid) load ?
Atrial Naturetic Peptide
Why are patients with CKD unable to concentrate their urine ?
increased water and solute excretion and loss of the medullary concentrating gradient from fibrosis lead to dilute urine.
What is the Urine Specific Gravity associated with the decreased urine concentrating ability of the nephron ?
Urine Specific gravity = 1.010 (isosthenuria)
What occurs to most patients with CKD at night ?
List the Anatomic Renal Adaptations in CKD
Hypertrophy of surviving structures, both glomeruli and tubules