Kidney Stones

Question 0

What are some other sites/causes of urinary tract obstruction apart from renal calculi?

Answer 0

Retroperitoneal fibrosis of ureter

Neuropathic bladder

Hypertrophy of bladder neck

Benign prostatic hypertrophy/prostate cancer

Urethral stricture

Question 1

What are the common locations for kidney stones to obstruct the urinary system?

Answer 1

Pelvic-ureteric junction

Iliac bifurcation point (where ureters cross pelvic brim)

Point at which ureters pass into bladder wall

Question 2

What are some of the causes of hypercalcaemia? What are the signs and symptoms associated with hypercalcaemia?

Answer 2

Primary hyperparathyroidism (measure [PTH]plasma)
Haematological malignancies
Non-haematological malignancies

note: in cases due to malignancy, hypercalcaemia has a rapid onset, suppressed [PTH]plasma, and rarely results in renal calculi

S&S: 
GI: 
- anorexia 
- nausea/vomiting 
- constipation 
- acute pancreatitis (rare)
CARDIOVASCULAR: 
- hypertension 
- shortened QT interval 
- increased sensitivity to digoxin 
RENAL: 
- polyuria & polydipsia 
- nephrocalcinosis (occasionally) - calcium deposits in kidneys 
CNS: 
- cognitive difficulties & apathy 
- depression 
- drowsiness -> coma 

[Ca2+] > 3.5mmol/l <— EMERGENCY

Question 3

What are some of the different types of hyperparathyroidism?

Answer 3

PRIMARY: increased [Ca2+]plasma (usually only one of the four parathyroid glands is enlarged)

SECONDARY: reduced or normal [Ca2+] e.g. vitamin D deficiency balancing increased [Ca2+]plasma

TERTIARY: increased [Ca2+] after longterm changes to parathyroid glands, leading to increased PTH secretion

e. g. renal failure -> vit. D not activated -> increased PTH secretion from glands -> kidney transplant required
e. g. vit. D deficiency -> increased PTH secretion -> vit. D deficiency “treated”

Question 4

How can malignancies cause hypercalcaemia?

Answer 4

Secretion of PTHrp (not measured by PTH lab tests)

+ cytokines e.g. TNF, IL-1
+ TGF-alpha
+ prostaglandins

Question 5

How is hypercalcaemia managed?

Answer 5

Hydration (IV saline)
Loop diuretics e.g. furosemide (NOT thiazides -> increased calcium reabsorption in kidney)
Bisphosphonates (inhibits osteoclasts -> reduced calcium reabsorption from bone)
Treat underlying condition

Question 6

How do renal calculi tend do manifest?

Answer 6

Incidental e.g. unrelated abdominal X-ray

Haematuria - painful (painless haematuria indicates malignancy)

Pain & associated complications of an obstruction in the renal tract

Question 7

What are the common types of renal calculi? In general, why do renal calculi form?

Answer 7

Calcium phosphate/oxalate (70%-80%)
Magnesium ammonium phosphate (5%-20%)
Urate (gout, chemotherapy) (5%-10%)
Cystine (2%-5%)

Increase in [stone-forming chemical] (supersaturation) —> crystallises & reduces urine volume

Reduced ionic strength reduces the risk of crystal formation e.g. K+ v.s. Ca2+

Reduced pH increases renal tubular reabsorption, which increases the risk of crystal formation

Reduced citrate synthesis increases risk of crystal formation (citrate inhibits calcium oxaloacetate/phosphate stone formation)

Question 8

What medical conditions are associated with the formation of different renal calculi?

Answer 8

Causes of hypercalcuria:

• absorptive (intestinal) —> increased calcium absorption means increased calcium excretion by kidneys
• renal —> reduced calcium reabsorption —> increased calcium excreted by kidneys

Causes of hyperuricaemia: gout, chemotherapy (note: ethanol competes with uric acid excretion)

Calcium oxalate stones: hypercalcuria, increased oxalate consumption, ileostomy, hyperuricaemia
Calcium phosphate stones: primary hyperparathyroidism, renal tubular acidosis (bone dissolves -> increase in [Ca2+]plasma)
Urate stones: hyperuricaemia
Triple phosphate stones: chronic UTIs
Cystine stones: cystinuria

Question 9

What are the investigations required when renal calculi are suspected?

Answer 9

History: ?underlying predisposing conditions, ?dietary excess/inadequate fluid intake/excessive fluid loss, ?medications

Bloods: levels of calcium, PTH, phosphate, urate + U&Es +acid/base status

Urinalysis: pH, sediments, culture (urea-splitting organisms)

Radiograph:

• radiopaque = calcium oxaloacetate/phosphate, cystine
• radiolucent = urate
• intravenous pyelogram (IVP)

Analyse stones

Question 10

What is the general and specific management of renal calculi?

Answer 10

Increase fluid intake, restrict dietary oxaloacetate & sodium (& possible calcium and protein), and refer to urology for surgery

Calcium stones: sodium cellulose phosphate/thiazides (renal hypercalcuria) —> reduces [Ca2+]
Urate stones: allopurinol —> reduces [urate]
Low citrate —> potassium citrate —> increases [citrate]

Question 11

What forms does calcium take in the plasma, and in what percentages?

Answer 11

45% ionised

45% bound to protein (80% of which to albumin)

10% complexed e.g. citrates, phosphates

Question 12

Where does calcium and phosphate reabsorption occur, and in what percentages?

Answer 12

PCT (NCE):

• ~60%-70% Calcium
• ~75%-80% Phosphate (inhibited by PTH)

Thick ascending limb of loop of Henle: ~20% Calcium

DCT:

• ~9% Calcium (stimulated by PTH)
• ~10% Phosphate

Collecting duct: ~1% Calcium

Excreted:

• ~1% Calcium
• ~10% Phosphate

reminder: calcitonin has little effect on [Calcium]serum/bone, but calcitriol has the opposite effect to PTH