Chronic Kidney Disease Flashcards
What is CKD?
Chronic kidney disease is best thought of as a loss of functioning nephrons.
Decreased functioning nephrons leads to decreased GFR and thus, elevated creatinine and BUN for 3+ months
What are stages of CKD?
1-5 based on eGFR
What are the high risk factors for developing CKD?
- diabetes
- HTN
- cancer
- GI tumors
- etc.
What are the limitations of using serum creatinine as a marker of GFR?
Serum creatinine will slightly over-estimate true GFR because it is secreted AND
as you lose nephrons, the other nephrons can compensate so the GFR will remain high even though there is significant nephron loss occurring
What are some requirements of using formulas to estimate GFR in CKD?
the Pcr must be constant over a significant time period to estimate
NOTE: these formulas account for age, gender, and ethnicity- all factors that influence the GFR
What is the Cockroft-Gault formula for estimating GFR?
(140-age)/Scr*(0.85)- if female
can only be used in a steady state condition (CKD). acute renal failure would not be considered steady state
How is stage 1 CKD defined?
GFR over 90
How is stage 2 CKD defined?
GFR 60-89
How is stage 3 CKD defined?
GFR 30-59
How is stage 4 CKD defined?
GFR 15-29
How is stage 5 CKD defined?
GFR less than 15 or dialysis
T or F. Serum creatinine is always a sufficient method to determine what stage of CKD a patient is in
F. Always have to take into account the demographics of the patient. For instance, a 20 yo AA male with Pcr of 1.3 may be stage 1 but a 20 yo WF with Pcr may be stage 2, etc.
Remember CKD would be a patient with elevated creatinine for 3+ months
Remember CKD would be a patient with elevated creatinine for 3+ months
What are some things you may want to ask a patient with CKD?
Are you having problems voiding urine? If yes, could point to obstructive uropathy
Is your urine abnormal?
Past medical history
What things would you be looking for upon physical exam of a patient with CKD?
- HTN
- flank masses (could suggest PKD)
- edema
A small kidney on ultrasound would indicate what?
chronic disease (9-12 cm normal)
What are some ways kidney disease must be differentiated?
- prerenal, intrinsic, postrenal
- acute or chronic
- glomerular or tubular
- inflammatory or non-inflamm
- with or w/out systemic disease
What things favor CKD over ARF?
patients will have high creatinine and will be less likely to be symptomatic (less N/V)
- presence of peripheral neuropathy (non-specific- diabetes)
- bone changes consistent with longstanding 2ndary hyperPTH
- small echogenic kidneys on ultrasound
- waxy casts on urinalysis
What factors favor tubular vs. glomerular etiology of CKD?
- absence of heavy proteinuria
- inability to concentrate or dilute the urine
- hyperkalemia and metabolic acidosis
So what urine SG would suggest tubular etiology of CKD?
~1.010 (Uosm= 300mOsm/kg)
What is the best test to differentiate between glomerular and tubular etiology?
urinalysis
What things on urinalysis suggest glomerular etiology?
2+ proteinuria,
red cell casts
SG greater than 1.015
What is the most common cause of eosinophils in the urine?
allergic interstitial nephritis (but if its not there, this could still be the diagnosis)
What will urinalysis of AIN look like?
sterile pyruia (negative culture)
T or F. Both glomerular and tubular diseases, whether inflammatory or non-inflammatory can lead to impaired renal function
T.
T or F. CKD tends to progress even if underlying causes are treated and/or removed completely
T.
What is uremia?
translates to urea in the blood but it is a term to describe the signs and symptoms associated with advanced renal failure include early morning N/V, anorexia
Uremia is 100% fatal unless what?
- reversible factors are ID’d or
- renal replacement therapy is started
Just about everyone with CKD will have complications of what?
- HTN
- CV disease
- CKD-metbaolic bone disease
- anemia
- metabolic acidosis
What is the most common cause cause of CKD? Other very common causes?
- diabetes mellitus
- HTN nephrosclerosis
- acute and chronic glomerular disease
- PKD
How do kidneys respond to nephron loss?
hypertrophy and hyper filtration of glomeruli, epithelium and endothelium
Thus, a 50% decrease in renal mass only results in 20-30% reduction of GFR
What causes accumulation of hyaline in renal injury?
epithelial cell injury causes proteinuria which causes hyaline to accumulate and cause expansion of the mesangial matrix leading to reduced capillary surface area for GFR
What does the expansion of the mesangial matrix also cause?
it unstableness the vascular capillary leading to microaneurysms
A greater than 50% loss of nephron loss results in what?
loss dependent increased risk of HTN, proteinuria (FSGS)
particularly when present 10+ years
The intact kidney hypothesis suggest that remaining kidney nephrons will compensate for the loss of other nephrons. But there must be some trade-off. What is it?
The body must work harder to maintain serum levels of things like Ca/Pi leading to hyperPTN and Na+ leading to HTN
Also, increased kidney work will eventually lead to further damage to the nephron
How can we prevent increase nephron loss in CKD?
- restrict protein intake
- control HTN (present in 85-90% of CKD patients)
Why would restricting protein intake help?
protein intake normally increases GFR transiently, thus increasing the workload
What is the difference between HTN in CKD and essential HTN in a normal)is) population?
the HTN in CKD is volume driven so salt intake is very beneficial while essential HTN has normal volume statue (until GFR becomes depressed)
In proteinuric disease, ACEIs and RBCS are advantageous. Why?
They not only reduce systemic pressure, but glomerular capillary pressure as well, thus reducing the hyper filtration to protect the kidneys from further scarring and further proteinuria (NDHP CCBs may have some similar effect)
other anti-hypertensives won’t have this effect
What does AngioII do to glomerular arterioles?
constrict efferent and dilates afferents to increase GFR
also increases TFG-B, promoting fibrosis
How common is diabetes induce nephropathy?
very, up to 30% in type I and similar in type II
What are some of the early changes seen in DN?
hyperfiltration resulting in glomerular capillary HTN and hypertrophy (thus, ultrasound shows enlarged kidney). As this process continues you will see signs of microalbuminuria and eventually proteinuria (+ dipstick), reduced GFR, and then systemic HTN
Histology of DN?
- increased mesangial matrix
- glomerular collapse
- glomerulosclerosis
How does CKD affect the heart?
-left ventricular hypertrophy causing CHF that can lead to a pericardial friction rub in advanced settings (dialysis needed at this point)
How does CKD affect the nervous system?
- subtle intellectual changes (cant focus) early
- overt encephalopathy can manifest (as asterixis) with more severe renal failure
- distal sensory peripheral neuropathy with advanced renal insufficiency
How does CKD affect the endocrine system?
Hypoglycemia due to decrease insulin degradation and decreased gluconeogenesis by the kidney (plus appetite is diminished a little)
Why is CKD associated with anemia?
Diminished production of EPO
When does anemia occur in CKD?
When GFR is approximately 30% normal (not much change in WBC or platelets)
Does the anemia in CKD respond to exogenous EPO?
Yes
What can EPO do to BP?
increases it (need to monitor)
How does CKD affect the GI system?
- decreased appetite
- non-food related N/V in mornings
