Term
| what is renal insufficiency? renal failure? |
|
Definition
| renal insufficiency: a measurable reduction in renal function. renal failure: a further reduction to the point that biochemical homeostasis cannot be maintained |
|
|
Term
|
Definition
|
|
Term
|
Definition
| symptoms of kidney failure |
|
|
Term
|
Definition
| less than 400 mL of urine/day |
|
|
Term
|
Definition
| less than 100 mL urine/day |
|
|
Term
| what is chronic kidney disease defined as? |
|
Definition
| kidney damage for 3+ months, as defined by 1) structural or functional abnormalities (even if GFR is normal) manifested by: pathologic abnormalities, markers of kidney damage (blood/urine testing/imaging techniques) OR 2) if GFR is <60 for 3+ mo with or without kidney damage |
|
|
Term
| what are the current stages for CKD? |
|
Definition
| stage 1: GFR >90, stage 2: GFR 80-60, stage 3: GFR 59-30, stage 4: GFR 29-15, stage 5: renal failure/dialysis/GFR <15. stage 1-2 are not really a problem, other than the fact that they lead to 3,4,5 |
|
|
Term
| are rates of CKD in the US increasing? |
|
Definition
|
|
Term
| how do CKD and CHF compare in terms of % of total medicare budget? |
|
Definition
|
|
Term
| what is the link between CVD and CKD? |
|
Definition
| risk of CVD is increased up to 2x w/creatinine 1.4-1.5 or microalbuminuria (between 30 and 300 is microalbuminuria). annual mortality from CVD is incresaed 100x w/kidney failure |
|
|
Term
| are certain ethnic groups more susceptible to developing CKD? |
|
Definition
| yes, african americans are a higher risk for ESRD (end stage renal disease), potentially due to the fact that DM and HTN are more prevalent in this population |
|
|
Term
| what is the intact nephron hypothesis? |
|
Definition
| the concept that each nephron is either a fully functional unit or does not function. surviving nephrons can increase their functional capacity by undergoing hypertrophy |
|
|
Term
| what is the general progression of CKD? |
|
Definition
| basically anything that changes total nephron mass will be associated with CKD progression. the intact nephrons will vasodilate, increasing protein/blood sugar intake along with pressure resulting in glomerular hyperfiltration and increasing membrane permeability. this leads to increased protein flux – albuminuria, which can cause mesangial cell injury, leading to cellular proliferation, followed by glomerular sclerosis (endpoint of all these injuries) |
|
|
Term
| what are the six mechanisms of renal disease progression? |
|
Definition
| 1) persistent glomerular injury leading to glomerular HTN and increased single nephron GFR 2) protein leak increasing angiotensin II 3) downstream cytokine bath 4) neutrophils, then macrophages, T cells leading to interstitial nephritis (*even though glomerular filtration rate is going down, much of pathology is in the interstitial areas) 5) tubular epithelium respond by detaching from BM and forming new interstitial fibroblasts 6) surviving fibroblasts lay down collagenous matrix, disrupting adjacent tubules and surrounding vessels - leaving an acellular scar |
|
|
Term
| what characterizes the pathogenesis of albuminuria in terms of nephropathy? |
|
Definition
| the BM becomes less anionic, and is less able to repel proteins (also anionic), capillary pressure increases, the mesangium expands, the glomerular capillary BM thickens, and interstitial fibrosis occurs - further compromising blood flow |
|
|
Term
| are lipids contributing agents to CKD? |
|
Definition
| yes. oxidized LDLs, LpA impair endothelial function and attenuate vascular tone and oxizides lipoproteins stimulate O2 production which inactivates NO |
|
|
Term
| how does angiotensin II contribute to renal disease? |
|
Definition
| angiotensin II will increase intraglomerular pressure, SMC proliferation, mesangial cell proliferation, Na+ reabsorption, activation of inflammatory transcription factor NF-kB, vascular endothelial cell proliferation, transforming growth factor beta, nephrosclerosis/interstitial fibrosis, ECM levels, expression of vasoactive factors, and aldosterone (therefore, a lot of therapy is aimed at reducing angiotensin II) |
|
|
Term
| what are the effects of high aldosterone levels, such as those seen in CKD? |
|
Definition
| aldosterone increases: K loss, Na retention, plasminogen activator inhibitor 1 (decreased fibrinolysis), proinflammatory COX-2/osteopontin, norepi, endothelial dysfunction, and decreases vascular compliance. *this all leads to an increased risk of: stroke, renal failure, and CAD/MI (major culprit in progression of disease) |
|
|
Term
| what are reversible conditions that may eventually lead to chronic renal failure? |
|
Definition
| anatomic, obstructive, vascular, HTN, RAS, and infection |
|
|
Term
| what are reversible conditions that may quickly lead to chronic renal failure? |
|
Definition
| increased Ca++, increased uric acid, decreased K+, primary glomerulopathies, nephrotoxins, vasculitis, and connective tissue diseases |
|
|
Term
| what are conditions that may aggravate chronic renal failure? |
|
Definition
| acidosis, CHF, increased Ca++, HTN, infection, decreased K+, obstruction, hypotension, hypovolemia, pericardial effusion/tamponade |
|
|
Term
| is PTH an important mediator of CKD? |
|
Definition
| yes, there is increased tubular PO4 which cuts down 1-alpha-hydroxylase activity (=less active 1-25-dihydroxy vitamin D), which stimulates hyperPTH via gene transcrption b/c of decreased calcitriol and subsequent increased PTH gene transcription (secondary hyperparathyroidism) |
|
|
Term
| what is the trade off hypothesis? |
|
Definition
| a description of how hyperparathyroidism occurs in CKD: *every time the GFR drops - PO4 levels increase*, causing Ca++ levels to drop. decreased Ca++ causes increased PTH, which raises Ca++ again, and levels out PO4, until the next GFR drop. this keeps everything pretty even, but just includes a progressive decrease in GFR and increase in PTH |
|
|
Term
| what are the consequences of secondary hyperparathyroidism? |
|
Definition
| renal osteodystrophy, myopathy, dermatological manifestations, neurological manifestations, anemia, CHF, and *vascular calcification* |
|
|
Term
| what are some of the skeletal manifestations of hyperparathyroidism? |
|
Definition
| rugger jersey spine, calvaria, demineralization of the skull, lost lamina dura of teeth, subperiosteral bone reabsorption in fingers, loss of distal clavicle (radiolucent) -> all due to Ca++ loss |
|
|
Term
| how is soft tissue affected by hyperparathyroidism? |
|
Definition
| deposits of calcium phosphate salts in the kidney, lung, the eye (keratinopathy), and vasculature |
|
|
Term
| how is hyperparathyroidism secondary to CKD treated? |
|
Definition
| phosphate binding compounds: calcium supplements (calcium carbonate and calcium acetate) or non-calcium supplements (sevelamer, lanthanum), vit D supplements (do decrease stimulation of PTH secretion, but can raise Ca++ levels), and cinacalcet (calimimetic agent that mimics the affects of elevated Ca++ levels - fairly effective in dropping PTH) |
|
|
Term
| what are CV manifestations of CKD? |
|
Definition
| accelerated ASCVD, HTN, CMP, LVH, and pericardial disease |
|
|
Term
| what are the hematologic consequences of chronic renal failure? |
|
Definition
| *anemia (due to decreased RBC production/decreased erythropoietin, marrow fibrosis, Fe/folate deficiencies, inhibitors), hemolysis, blood loss, bleeding tendencies (platelet dysfunction/anemia), and altered neutrophilic chemotaxis/depressed lymphocyte function |
|
|
Term
| what are neurologic manifestations of CKD specific to the CNS? |
|
Definition
| CNS: decreased level of consciousness, sleep reversal, coma, decreased memory, decreased attentiveness/cognitive tasking, asterixis, myoclonus, and seizures |
|
|
Term
| what are neurologic manifestations of CKD specific to the PNS? |
|
Definition
| peripheral neuropathy, singultus, muscle fatigue, and muscle cramps |
|
|
Term
| are pulm manifestations of CRD significant? |
|
Definition
| not really, but atypical pulm edema, pneumonitis, and pleuritis are possible |
|
|
Term
| what are GI manifestations of CRD? |
|
Definition
| anorexia, N/V, stomatitis, parotitis, gastritis, enterocolitis, and pancreatitis (rare, but lethal) |
|
|
Term
| what are dermatological manifestations of CRD? |
|
Definition
| uremic calcific arteriolopathy/calciphylaxis - causes necrosis of the skin and kyrle's disease (hyperkeratosis follicularis), not lethal, but itchy and common |
|
|
Term
| what are endocrinological manifestations for CRD? |
|
Definition
| secondary hyperparathyroidism, carb intolerance (due to insulin resistance, vit D derivatives can help), type IV hyperlipidemia, altered thyroxine metabolism, testicular atrophy, and ovarian dysfunction (most pts are sterile) |
|
|
Term
| how is acid-base regulation affected by CRD? |
|
Definition
| impaired excretion of PO4, sulfates. decreased ammonia synth. impaired bicarb reabsorption. decreased distal H+ secretion. and reduced excretion of titratable acid = all this can be improved with bicarb (HCO3) supplementation |
|
|
Term
| what are tx considerations for CRD? |
|
Definition
| ACE inhibitors, ARBs, renin antagonists, (all these address HTN, proteinuria, DM), aldoesteron antagonists, erythropoietin, & diet (protein, phosphorus restriction). (**regardless of reason for kidney disease, aggressive blood pressure control – for blood pressures around 120/70ish is the most important thing that can do) |
|
|
Term
| what does renal replacement therapy consist of? |
|
Definition
| dialysis (hemodialysis or peritoneal dialysis) or transplantation |
|
|
Term
| what does peritoneal dialysis do? |
|
Definition
| uses your own peritoneal membrane to dialyse blood |
|
|
