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Renal Response to Nephron Loss - Coggle Diagram
Renal Response to Nephron Loss
Decreased GFR
Characteristics
Hypervolemia
Hyperphosphatemia/hypocalcemia
Acidosis
Hyperkalemia
Anemia
Hyperlipidemia
Hypertension
Uremia
Accumulation of substances normally removed by the kidneys, many are small and water soluble but some are fat soluble
Adaptation
Solute Removal
Levels Begin to increase as GFR falls: urea and Creatinine
Levels stable till 50-70% of loss of GFR: Ca++, PO4--
Levels stable till 75%-90% of loss of GFR: K+, Na+, H2O
Nephron Damage
Intact Nephron Hypothesis
Ability of remaining nephrons to function essentially as intact nephron units
Changes in hemodynamics can increase GFR
Dilation of remaining nephrons occurs which causes increase in intraglomerular capillary pressure and flow
Resulting Functions
Increase in GFR in remaining nephrons, Increase solute removal per nephron
Increased number of tubular transporters
Solute Control
Potassium
Increase tubular flow due to increased GFR of each remaining nephron
Increased Cellular transport due to flow and growth of tubules
Calcium and Phosphate
Low plasma calcium results from
Decreased GFR which leads to increase in plasma phosphate since less phosphate is filtered
Decrease in 1-25 OH-D3
Low calcium and high phosphate result in: Increased parathyroid hormone
Increased bone osteoclast activity and decreased phosphate reabsorption from proximal tubule
Tradeoff Hypothesis
With falling GFR, there is a rise in PTH stimulated by rise in PO4 and drop in CA++
Leads to increase in Ca++ released from bone, decreased reabsorption of PO4 by renal tubules
Plasma Ca++ and PO4 stay near normal until GFR falls very low
Progression of Renal Failure
CKD and low GFR have most of nephrons affected by the renal disease causing CKD
Worsening GFR occurs over time even if remaining neprhons were normal at time of nephrectomy
Sclerosis of Segments of previously normal glomeruli
Altered Glomerular Hemodynamics
Decreased neprhon number and decreased GFR
dilation of afferent arterioles increaseing intraglomerular flow adn pressure
Treatment
BP Control
ACE Inhibitors/ARBs
Can cause further decrease in GFR leading to hyperkalemia
SGLT2 Inhibitors
Activate tubuloglomerual feedback part of nromal autoregulation
Inhibits sodium and glucose reabsorpption at proximal tubule
Results in increased sodium at macula densa and signalling to afferent arteriole to constrict
Protein Restriction
Leads to less afterent arteriolar dilation
