Urinary System disease

Question 1

Renal failure (RF) + causes

Answer 1

• RF is commonly described as a decrease of GF, although it can also affect endocrine function
• RF has occurred when the functioning of the kidneys is disrupted to the extent that normal excretory function is inadequate to reduce waste sufficiently to maintain homeostasis.
• Consequences:
  1. Reduced elimination of wastes (eg. urea, uric acid, creatinine).
• often measured by blood serum creatinine levels = if too high = RF
• reduced elimination of H+
  ( → metabolic acidosis) + K+ ( → cardiac failure)
  2. Endocrine effects
• bone disease (reduced production of calcitriol)
• anaemia (reduced production of EPO)

Question 2

Grades of renal failure

Answer 2

• Recall – there are ~ 1 mil nephrons per kidney → kidneys have a large reserve capacity
• Usually no symptoms of renal disease until >75% of nephrons are lost.

Grades of renal failure:

1. Renal insufficiency (70-75% loss of nephrons):
   - decline in renal function: plasma, urea, uric acid, creatinine levels raised, but patients generally asymptomatic
2. Mild renal failure (>75% loss of nephrons)
   - symptoms start to show: disturbances in water + electrolyte balance, mild acidosis.
3. End stage renal disease: (>85% loss of nephrons).

Question 3

Causes of renal failure

Answer 3

• Because no new nephrons are made after birth, gradual nephron loss is normal w/ aging. However the degree of nephron loss should be insufficient to cause symptoms over a 100 yr life span
  CAUSES:
  1. Infectious organisms:
  kidney infection; either blood born, or via urinary tract.
• nephrons damaged, no recovery.
  2. Toxic agents: lead, arsenic, insecticides, overdose or long term exposure to aspirin or ibuprofen (NSAIDs).
• nephrons damaged, no recovery.
  3. Low renal artery flow:
• reduced glomerular blood flow → reduced GFR
• acute or chronic
  - acute: circulatory shock, haemorrhage, acute low BP
  - chronic: heart failure, renal artery stenosis/ atherosclerosis
• nephrons not damaged, recovery.
  4. Obstruction of urine flow:
  such as kidney stones. This leads to back pressure, increasing Bowman’s capsule pressure, & net filtration pressure is reduced.
• nephrons not damaged, recovery

Question 4

Renal Dialysis: Haemodialysis

Answer 4

• Renal dialysis is a medical procedure that can supplement or replace normal kidney function.
• Two forms: haemodialysis + peritoneal dialysis.
• Blood is pumped through a fenestrated tube that is bathed in dialysis fluid which has similar properties to plasma (not identical).
• aim is to generate appropriate conc. gradients.
  eg dialysis fluid contains normal [glucose], so no diffusion of glucose from blood; but low [urea] so urea will diffuse out of blood.
• Takes 3-5 hours/day for 3 days/week

Question 5

Peritoneal Dialysis

Answer 5

• W/ peritoneal dialysis, the dialysate is circulated through a catheter inside part of the patient’s peritoneal cavity
• The peritoneum is used as the dialysis membrane through which dialysate fluid is exchanged w/ the blood.
• This treatment can be done at home, or while traveling.
• Has better outcomes than hemodialysis during the first couple of years.
• Requires greater capacity for care at home.
• greater risk of infections

Question 6

Why is dialysis not a perfect replacement for the kidney?

Answer 6

• Dialysis is an imperfect treatment to replace kidney function because it does not correct the endocrine functions of the kidney.

Question 7

Kidney Transplant

Answer 7

• Surgical implantation of a new kidney can come from either a living donor (~60%) or cadaver (40%)
• The recipient’s non-functioning kidneys are normally left in place, because outcomes have been shown to be better.
• Can support both the excretory + endocrine functions of the kidney.
• The success rate depends on the recipient’s immune response against the donated kidney

Question 8

Renal Tubular Acidosis (RTA)

Answer 8

• Genetic disorders leading to accumulation of acid in the blood due to failure of kidney to secrete enough acid or to reabsorb enough bicarbonate.
• Typically problem function of H+ or HCO3- pumps/ transporters
• Two causes:
  (i) proximal RTA: insufficient (R) of bicarbonate ions in the PT
  (ii) distal RTA; insufficient secretion of acid (H+) into the DT
• Chronic acidity of the blood leads to growth retardation, bone demineralisation
• Chronic alkalinity of the TF leads to precipitation of Ca3(PO4)2 → nephrocalcinosis (kidney stones)
• Associated with ↓[K+] blood (hypokalaemia)
• note opposite to normal metabolic acidosis
• Can be treated by giving oral bicarbonate

Question 9

Renal hypophosphataemia

Answer 9

• Also known as “vitamin D resistant rickets”
• Most commonly as an inherited X-linked dominant trait in children.
• Characterized by soft, bendable bones due to low levels of phosphate in the blood (but calcium levels are normal)
• Osteoid production occurs but mineralization of osteoid (mature bone) is inadequate.
• osteoid is the unmineralised collagen portion of bone matrix that forms prior to maturation of bone
• More and more bone is made up of collagen matrix without a mineral covering, so the bones become soft.
• Failure of phosphate (R) in nephrons (especially PT; cotransport w/ Na+)