1. Proximal Convoluted Tubule Active Reabsorption –Nutrients (glucose, amino acids, Vitamins) –Ions (K +, Na +, Cl -, Ca 2+ ) –Small plasma proteins –Some urea and uric acid ~70% of Filtrate is reabsorbed in PCT Question: How are these Reabsorbed?

2. Reabsorption of Na + : First – simple diffusion: Then – 1 o active transport: Na + is Actively Reabsorbed:

3. Na + linked 2 o Active Transport Symport with: –Glucose –Amino acids –Ions (e.g., Ca 2+ )

4. Passive Transport of Water: –As Na + pumped out, H 2 O follows by osmosis. (passive) Transcytosis of Proteins: – Small proteins can get into filtrate, due to size they are reabsorbed via vesicular transport. Passive Transport of Urea: –As other solutes leave lumen, [urea] higher than ECF, thus passively diffuses into ECF.

5. Reabsorption of Urea

6. Transporter Characteristics A substance can exceed renal threshold, e.g., glucosuria. –Saturation (# of carriers): –Competition: –Specificity: glucose, fructose, tyrosine, valine, etc, all have own carriers. maltose instead of glucose – takes a seat, but not transported. limited # of carriers to transport solutes back into body.

7. First, Na + transported out of filtrate. H 2 O Reabsorption – Loop of Henle a key site. Collecting duct also a key site for H 2 O reabsorption – (role of ADH). Osmolarity of ECF gets higher. Deeper into medulla, more H 2 O drawn out. Filtrate becomes Very concentrated!

8. Region is impermeable to H 2 O. Ascending Loop of Henle Thus, H 2 O can no longer leave filtrate in this region, so Osmolarity becomes lower again at start of DCT.

9. Active Transport into nephron tubules e.g., K +, H + and HCO 3 - Secretion – DCT a key site. Fine-tuning - eliminate unwanted items. This filtrate in tubules is destined to be urine unless reabsorbed in collecting ducts.

10. Reabsorption of Na + Final Modification: Collecting Ducts After collecting duct, filtrate now called urine (no longer modified). Reabsorption of H 2 O Under Endocrine Control – ADH (vasopressin)

12. Mictruition Reflex

13. Autoregulation of Renal System

14. Renin-Angiotensin-Aldosterone

15. _______________________ ______________ (inactive) (_____________) _________________________________ ___________ ____________ (activated) _____ _______________ LiverKidneys Lungs Adrenal Cortex Na + _______ H 2 O _______ Thirst StimulationVasoconstrictionReabsorption of H 2 O Kidneys (active)

16. Anti Diuretic Hormone (ADH) Angiotensinogen (inactive) (Vasopressin) Angiotensin Converting Enzyme (ACE) Aldosterone Angiotensin I (activated) Renin Angiotensin II LiverKidneys Lungs Adrenal Cortex Na + retention H 2 O retention Thirst StimulationVasoconstrictionReabsorption of H 2 O Kidneys (active)

17. Comparison of Fluids PlasmaFiltrate Urine Blood Substance (parameter) Rate pH Osmolarity Cells Na +, K + Large Pro - Small Pro - Glucose Urea Volume

18. Renal Failure When kidney function disrupted to the point they are unable to perform regulatory and excretory functions sufficient to maintain homeostasis. Acute – sudden onset with rapid reduction in urine formation (less than 500ml/day minimum being excreted). Chronic – slow, progressive, insidious loss of renal function. Up to 75% of function can be lost before detected.

19. Normal Healthy Kidney

20. Polycystic kidneys

21. Enlarged Polycystic kidneys (16 to 18 pounds combined).

22. 1. Infectious organisms. Variety of Causes of Renal Failure: 2. Toxic agents. 3. Inflammatory immune response (allergic). - Blood borne microbes - UTI’s - lead, arsenic, pesticides, additives, medications - long-term exposure to high aspirin doses - glomerulonephritis, sepsis - e.g., after strep throat (streptoccocus)

23. Variety of Causes: 4. Obstruction of urine flow. 5. Insufficient renal blood flow. - Kidney stone (calcium oxalate, uric acid crystals) - Tumors - Enlarged prostate gland All create back pressure, decreasing GFR - 2 o to heart failure - Hemorrhage (e.g. shock) - Atherosclerosis Leads to inadequate Filtration pressure

25. 1. Uremic Toxicity Potential Ramifications: 2. Metabolic Acidosis 3. Potassium (K + ) retention - Caused by retention of toxins/waste products in blood. - From inability of kidneys to secrete H +. - Inability to secrete K + (effects RMP).

26. 4. Na +, Ca 2+ and phosphate and Imbalances 5. Loss of plasma proteins 6. Anemia - Inability of kidneys to regulate ion reabsorption and secretion. - Result of increased leakiness of glomerulus. - Inadequate erythropoiten production. 7. Depressed immune system - Increased toxic waste and acidic conditions.

27. Possible Treatments for Renal Failure: Dialysis Kidney Transplant Stop or Treat the Cause

28. Overall Processes of the Nephron