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Flashcards in chronic kidney disease Deck (23):
1

Define chronic kidney disease

a permanent reduction in glomerular filtration rate (GFR)

2

1. 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

3

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

4

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.

5

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

6

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

7

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.

8

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

9

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

10

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

11

Define uremia

clinical syndrome resulting from retention of certain substances that are normally excreted into the urine and thus accumulate causing toxicity.

12

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.

13

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

14

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

15

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

16

Three regulators of parathyroid horomone

Calcium, 1,25 Vitamin D, phosphorus

17

Calcium sensing receptor and PTH

The calcium sensing receptor is a transmembrane receptor that senses extracellular free calcium. When calcium is bound to the receptor it results in a decrease in PTH release and a downregulation of PTH production

18

Actions of 1,25 Vitamin D and its relation to PTH

Vit D actions include stimulating the absorption of calcium and phosphorus from the intestine; and at the level of the parathyroid gland down-regulates PTH gene transcription. As GFR falls, renal production of 1,25 Vit D falls, resulting in decreased phosphorus/calcium absorption, and increased PTH production

19

Actions of FGF-23

Phosphorus regulatory hormone produced by osteocytes in bone and causes phosphaturia (increased phosphorus excretion) and decreases the kidneys production of 1,25 vitamin D, presumably as a compensatory mechanism to prevent phosphorus overload.

20

Is renal disease progressive?

yes

21

Why is renal disease progressive?

Dilation of afferent arteriole occurs to increase GFR, and this increased flow/pressure (hypertension) leads to destruction of the glomerulus. Also, increased oxygen consumption by remaining nephrons occurs

22

Prevention of chronic kidney disease progression

No therapy can completely stop. ACE/ARBs slow progression by controlling BP, treatment of metabolic acidosis, treatment of Vitamin D deficiency

23

Teatment of CKD

Treat uremia with hemodialysis, peritoneal dialysis and renal transplantation