chronic kidney disease Flashcards
Define chronic kidney disease
a permanent reduction in glomerular filtration rate (GFR)
- Understand the stages of chronic kidney disease and the utility of this classification system
Stage 1: kidney damage with normal GFR (>90), diagnosed and treated. Stage 2: kidney damage with mildly decreased GFR (60-89), estimate progression. Stage 3: moderate decreased GFR (30-59), treat complications. Stage 4: severe decreased GFR (15-29), prepare for renal replacement therapy. Stage 5: kidney failure (GFR <15 or dialysis), dialysis or transplant
Most common causes of chronic kidney disease
1) Diabetic nephropathy- most common 2) Hypertensive nephrosclerosis & Renal vascular disease 3) Glomerulonephritis 4) Polycystic kidney disease 5) Interstitial nephritis 6) Obstruction
Why is chronic kidney disease silent
Intact Nephron Hypothesis: Nephrons maintain glomerulotubular balance comparable to all other nephrons. That is, filtration and net excretion are coordinated.
The Magnification Phenomenon:nephrons magnify their excretion of a given solute. Individual Solute Control Systems: Each solute appears to have a specific control system that is geared to maintain external balance in CKD. Each solute system has individual tubular handling and hormonal influences.
Intact Nephron Hypothesis: Nephrons maintain glomerulotubular balance comparable to all other nephrons. That is, filtration and net excretion are coordinated.
The Magnification Phenomenon:nephrons magnify their excretion of a given solute. Individual Solute Control Systems: Each solute appears to have a specific control system that is geared to maintain external balance in CKD. Each solute system has individual tubular handling and hormonal influences.
Trade off hypothesis
Mechanisms that maintain individual solute control may have deleterious effects on other systems. Ie. Increased parathyroid hormone maintains normal serum calcium and enhances renal phosphorus excretion but can cause disturbances in sleep, sex. Bone disease, anemia, lipidemia, vascular disease
How are creatinine and urea balanced in chronic kidney disease
Passive: excretion rates for urea and creatinine remain constant in the face of diminished clearance. This occurs at the expense of elevated plasma concentrations
How is water balanced in chronic kidney disease
Active: In order to maintain balance, the fraction of water reabsorbed by the kidney must decrease. failing kidney cant concentrate/dilute urine, so max conc is 300mosm/L and max dilution is 200 mosm/L (compared to nl range of 50-1200). Since we make 600mosm of waste per day that must be removed, with maximal concentration 600mosm will be lost in 2 L of water.
How is sodium balanced in chronic kidney disease
Active: fraction of sodium reabsorbed must be decreased and the fraction excreted increased. A humoral natriuretic peptide helps to increase sodium excretion in CKD. Other mechanisms include volume expansion, increased tubular fluid flow rate, hyperfiltration in remaining nephrons, and local vasoactive substances
How is potassium balanced in chronic kidney disease
Outside control: Plasma and total body K are maintained on normal diet due to increased tubular secretion (as a result of increased tubular flow, increased solute load per nephron, increased Na delivery, increased aldo), until severe kidney disease, then fecal excretion
How is acid/base balanced in chronic kidney disease
3 forms of acid: H, NH4, PO4. When nephrons are lost the remaining nephrons increase their net acid excretion by increasing NH3 production and therefore their NH4+ excretion. This is limited, so metabolic acidosis is seen when kidney function falls below 25% normal
3 forms of acid: H, NH4, PO4. When nephrons are lost the remaining nephrons increase their net acid excretion by increasing NH3 production and therefore their NH4+ excretion. This is limited, so metabolic acidosis is seen when kidney function falls below 25% normal
Define uremia
clinical syndrome resulting from retention of certain substances that are normally excreted into the urine and thus accumulate causing toxicity.
Pathogenesis of uremia
retained metabolic products: nitrogenous products. Overproduction of counter-regulatory hormones: parathyroid hormone is producd in response to hypocalcemia and natriuretic hormone in response to volume overload. Underproduction of renal hormones: decreased EPO causes anemia, decreased 1-OH Vitamin D causes bone dz and secondary hyperparathyroidism.
Factors contributing to anemia from uremia
Decreased RBC production from decreased EPO, RBC survival shortened, blood loss secondary to decreased platelet function, marrow space fibrosis
Factors contributing to hypertension from uremia
Expansion of ECF volume due to reduced Na excretion, increased renin-angiotensin activity, dysfunction of ANS with insensitive baroreceptors, dimished vasodilators
Mineral bone disease
Altered calcium and phosphorous metabolism. Trade off hypothesis states that as the kidney fail phosphorus is retained which drives down the ionized calcium. This stimulates parathyroid hormone release which increases excretion of phsophate and restores calcium levels to normal. PTH levels continue to rise as GFR falls, until renal tubules cn no longer respond to PTH. Then hyperphosphatemia, hypocalcemia, bone disease, etc result
