Chronic Kidney Disease Flashcards
What defines End Stage Kidney Disease
once GFR is below 15 ml/min/1.73m^2
-at this point, consider dialysis or transplant
Risk Factors (4 non-mod and 6 mod)
- Non-modifiable
- Genetic, age, black or prematurity
- Modifiable
- DM, HTN, obesity, dyslipidemia, hyperuricemia, smoking
What is the general pathophysiology?
- Loss in # functioning nephrons NOT dec in functionality of individual nephrons
- Remaining nephrons compensate- hyperfiltration, hypertrophy, glomerular growth, etc
- Glomerular cap HTN - largely due to RAAS activation
- Mesangial cells multiply
- Epithelial cell hypertrophy
- Inc # epithelial cell foot processes
- Inc length of glomerular capillary
3 Steps of Glomerular Sclerosis
- 1- Endothelial injury and inflammation
- 2- Proliferation (stretched epithelial cells and proliferation/de-differentiation of mesangial cells)
- 3- Fibrosis (hyaline material accumulates in sub-endo regions of glomerulus –> collapse of capillaries –> glomerularsclerosis)
5 Ways to Stop CKD Progression
1- Early dx can slow progression - SCREEN
2- BP control- esp w/ ACEi or ARBs
creatinine
3- May dec protein intake
- Protein loads = hyperfiltration - BUT careful of malnutrition - Only has moderate efficacy
4- Smoking cessation
- Nicotine in renal artery = inc GFR - Also inc cortisol, aldosterone and catecholamines - Plus vascular effects
5- Avoid prescribing nephrotoxins
- NSAIDS, cyclosporine, IV contrast
Non-traditional Factors that put CKD Patients at CVD Risk
- anemia, vol overload, Ca/phos disturbances, hyper-parathyroidism, uremia, malnutrition, inflammation
Symptoms of Uremia
- Cardio - HTN, ischemic disease, pericarditis, CHF
- Endocrine - glucose intolerance, hyperlipidemia, infertile, sex dysfunction, secondary hyperparathyroidism
- Heme - anemia, bleeding diathesis
- Neuro/psych - peripheral neuropathy, CNS disturbances, seizures, sleep disorders
- GI - anorexia, nausea, vomiting, gastritis
- Immunological - leukopenia, lymphocytopenia, dec antibody response, inc susceptibility to infection
- Derm - pruritus, uremic pigmentation/frost, caliphylaxis, nail changes
- Muscle - carpal tunnel, myopathies, mineral and bone disease
How does regulation change in CKD kidneys?
- Maintain regulation of Na, K, H and water until very late in the disease (stable despite dec GFR)
- Maintain some regulation of phosphate and bicarb (so these change somewhat)
- Little regulation of creatinine, BUN or nitro waste (so these readily inc as GFR dec)
- Dec ability to make high Osm urine
CKD and Creatinine/Nitro Waste
- Maintain same daily excretion but at greater serum conc of creatinine and nitro waste
- Inc serum creatinine is proportional to dec GFR (good measure)
- Urea not as reliable b/c also influenced by catabolic state, protein intake, steroids, etc
CKD and Na+
- Adapt by inc fractional Na excretion (so if only filter small amount of Na you want to excrete a larger portion of that filtered Na)
- How? loop or thiazide diuretics, adaptive natriuresis (initial pos Na balance –> hypervol –> inc Na excretion) and ANF
- BUT CKD patients can only maintain these mechanisms at a small range of Na intakes so restrict Na intake (2 g/ day)
CKD and Water
- Dec GFR means less water filtered
- Comp by dec fractional reabsorption of water (so do not reabsorb as much of the filter as you normally do) –> dec ability to make conc urine
CKD and K+
- Less filtered (dec GFR) so more must be secreted in distal nephron
- Do so by… Inc aldosterone, inc extracellular K+, inc distal tubular flow
- Careful of sudden K+ load or meds that dec K+ secretion (ACEi or K-sparing diuretic) –> hyperkalemia
CKD and Acid/Base
- Metabolic acidosis; why?
- Less ammonium production b/c less functioning nephrons; less H+ leaving in form of ammonium in urine
- Also minor renal bicarb wasting - Early hyperchloremic (due to dec ammonium production - ABOVE)
- Late HAGMA (retain sulfates, phosphates, etc - “U” - uremia)
Anemia in CKD
- Dec erythropoietin production (normally made in kidney) –> deprives bone marrow of stimulus for RBC production
- Tx - synthetic erythropoietin or erythropoiesis-stimulating agents
- Risk of iron deficiency (give supplement), HTN, inc CVD risks if near normal; so only give if greatly reduced
Secondary Hyper-Parathyroidism
- Inc PTH Prod b/c …
1-As GFR dec, eventually serum phosphate inc –> stimulate PTH production
2- Inc phosphate –> Ca-phos deposits –> dec Ca++ –> also stimulates PTH production
3- Vit D converted into active form (calcitriol) in kidney so dec GFR –> dec calcitriol levels —> hypocalcemia –> stimulates production of PTH
- Inc PTH leads to inc phosphate excretion, renal Ca++ reabsorption & bone resorption (inc serum Ca) and inc synthesis of 1-alpha-hydroxylase which makes clalctriol in kidney
- BUT… in CKD there is PTH resistance and more phosphate retention and limited Vit D feedback so… even more PTH (secondary hyper-parathyroidism)
