Chronic Kidney Disease Flashcards
T or F: Creatinine lab values are great indicators of kidney function all of the time?
False, Creatinine may make kidney function appear more stable than it actually is
Why should you be weary of saying that a creatinine value of 1.0 g/dL is normal?
• You must take into account the PATIENT, a big ass athlete may have a normal creatinine of 1.5 g/dL while a little old man might have a normal of 0.6 g/dL
(YOU MUST take age, gender, and muscle mass into account)
Even in the absence of creatinine levels, what tests/findings can be indicative of CHRONIC kidney injury?
• SMALL trunckated (ECHOGENIC) kidney’s that are less than 9cm tells you that its a CHRONIC process
T or F: acute injury is more likely to be symptomatic than chronic injury
True
What is PATHOPNEUMONIC for glomerular damage leading to renal failure?
• what is a good indicator of tubular dysfunction?
GLOMERULAR:
• Red Blood Cell Casts**
• pts. will also have proteinuria
TUBULAR:
• Inability to concentrate the urine
What disease is often implicated with WBCs in the urine, but negative urine cultures?
ALLERGIC (and tubular) cause of Kidney Failure
What are the symptoms of uremia?
• what is the px. of CKD with uremia?
Symptoms:
• Nausea, Vomiting, Fluid Retention
Px:
• BAD prognosis, Kidney disease will kill these people
What creates Hyaline deposits?
• Hyaline - created from protein crossing podocytes
What are two VERY important factors we try to control in CKD?
HYPERTENSION
• this is pretty easy to control with drugs
SODIUM (=poison)
• harder to control
Why are ACE inhibitors and ARBs good for lowering proteinuria?
• why is important to lower proteinuria in CKD?
Why are they good:
• they PREVENT angiotensin II mediated constriction of the efferent arteriole (which increases intraglomerular pressure)
Proteinuria is a BAD px. indicator of CKD
Why do most people die before they can even get put on dialysis?
• pathophysiology?
CARDIOVASCULAR dysfunction secondary to kidney dysfunction
Pathophysiology:
• LV hypertrophy occurs from increased Na+ rentention leading to inc. ECFV (=> inc. preload => inc. afterload => hrt. failure)
UREMIA CAUSES PERICARDIDITIS
T or F: uremia is a strong indicator for dialysis.
True, you need to prevent pericarditis etc.
Why are people with CKD more likely to experience fasting fasting hypoglycemia?
Insulin is excreted in the kidney so people with CKD get a build up of serum insulin
What is one of the 1st symptoms of CKD?
• Early morning nausea (really just empty stomach nausea in general)
What is Calciphylaxis?
• when does this occur?
Calciphylaxis
• calcium lines and blocks up the blood vessels ultimately leading to skin breakdown and ulceration
This is a late stage probelm
What is the last mineral to become dysregulated in CKD?
•POTASSIUM
T or F: in CKD almost everyone starts to develop metabolic acidosis
True
What is expected in the following for CKD? • Hx • Physical Exam. • Lab data • Imaging Studies
Hx:
• Voiding Complaints
• Abnormal Appearance of urine
Physical:
• HTN
• Edema
Lab Data:
• elevated Creatinine and BUN
Imaging:
• Ultrasound
What are some key factors in determining if CKD is acute or chronic?
- Peripheral Neuropathy
- Bone Changes consistent with longstanding hyperparathyroidism
- Small kidneys on ultrasound
- waxy casts
What are 4 main factors that suggest Tubular Etiology of renal failure more so than Glomerular?
- Absence of Heavy Proteinuria
- Can’t concentrate urine (specific gravity 1.010 and osmolarity of ~300 mosm/kg)
- HYPERKALEMIA and Metabolic Acidosis out of proportion to renal insufficiency
What is THE MOST IMPORTANT component to differentiating glomerular and tubular disease?
Urinalysis
*lots of protein (2+), RBC casts, specific gravity greater than or equl to 1.015 suggest glomerular etiology
What pathology is typically associated with active inflammation of the tubules?
• glomerulus?
Tubulointerstitial Nephritis:
• Pyelonephritis
• Allergic interstitial nephritis
Glomerulonephritis:
• all of the Nephritic syndromes
T or F: Chronic kidney disease tends to be inexorably progressive, even if the initial injuring stimulus is removed
True
What are the most common etiologies of advanced kidney disease in the US?
- DIABETES MELLITUS*** #1
- hypertensive nephrosclerosis
- acute and chronic glomerular diseases
- polycystic kidney disease
- tubulointerstitial diseases
What is the renal response to nephron loss?
- Compensatory Glomerular Hypertrophy
- Compensatory Hyperfiltration
*50% decrease in renal mass results in only 20-30% reduction in GFR b/c residual nephrons pick up the slck
What are some side effects that increase in a dose dependent manner in response to loss in nephron mass greater than 50%?
- HTN
* Proteinuria
Compare HTN in CKD to 1º HTN.
CKD HTN is more often due to volume overload rather than
What is the best indicator of overall kidney function?
• how do we estimate this?
GFR - best index of overall kidney function
Estimate:
• via creatinine
Why might CKD progress even in the absence of original underlying disease?
Increased stress put on remaining nephrons could lead to kidney dysfunction
Is Diabetic Nephropathy more associated with Type 1 or Type 2 diabetics?
• why does diabetes lead to nephropathy?
Type I
Hyperfiltration Results in Glomerular Capillary HTN and Glomerular hypertrophy
Why are ACE inihibitors better than diuretics or direct vasodilators at preventing albuminemia?
They lower capillary pressure systemically (reducing afferent arterial flow) but ALSO act to vasodilate the efferent arteriole
Differentiate between the Trade off and Intact nephron hypothesis.
Intact Nephron Hypothesis:
• Damage nephrons generally function how they should so loss of renal homeostasis is 2º to a decreased number of nephrons
Chonic Kidney disease = decreased number of normally functioning nephrons
Trade Off Hypothesis:
• Secondary events occur to assist in homeostasis with the addition of adverse side effects
What are some of the compensatory changes made according to the trade off hypothesis?
Compensatory Changes:
• Calcium/phosphorus | secondary Hyperparathyroidism
- Na+ balance | HTN
- K+ balance | Hyperaldosteronism and HTN
- Remaining nephrons pick up the slack | increased filtration by resisdual nephrons causing injury
T or F: urinary flow rate is a good secondary marker of renal function
FALSE
What is a simple equation for estimating GFR by taking into accound age and sex?
(140 - age)/Creatinine x (0.85 - if female)
Describe the 5 stages of CKD.
- Kidney Damage with Normal or High GFR
- Kidney Damage with Low GFR
- Moderate low GFR
- Severe low GFR
- Kidney Failure
T or F: you should treat patients with CKD as if they are in the highest risk group for CVD.
True
What are some of the nervous system effects of CKD?
- Difficulty Concentrating
- Encephalopathy manifested by ASTERIXIS
- PERIPHERAL NEUROPATHY
How does HTN help to compensate for low GFR?
- Low GFR = less ability to filter Na+
- Na+ is retained
- HTN increases pressure natriuresis promoting ability to maintain Na+ balance
Why is CKD associated with anemia?
• when does this occur?
These people have significantly less blood cell synthesis b/c of less EPO
• Occurs at 30% of normal GFR
Why do people develop PROTEIN calorie malnutrition when they have CKD?
• They have a LOSS of APPETITE and concurrent decrease in protein intake
Why do people with CKD excrete increasing amounts of PTH?
- PHOSPHATE builds up
- Kidney is dysfunctional
Leads to…
• Down regulation of 1-alpha-hydroxylase and less Calcitriol production
which leads to…
• Increase PTH secretion
What derangements happen in phosphorus metabolism in CKD?
- PO4 complexes with Ca2+ leading to decreased serum Ca2+ conc.
- Inhibits 1-alpha-hydroxylase
- Metastatic Calcification
- Enhancement of PTH secretion
T or F: Potassium homeostasis can be maintained until GFR is below 15 ml/min
True
Do people with CKD tend to progess toward metabolic acidosis or alkalosis?
*Explain
Acidosis:
• decreased NH4+ production from decreased numbers of nephrons
This will be acidosis with normal ion gap
