Renal stones

Question 1

Describe the differences between primary and secondary ureteric reflux

Answer 1

Basically, the primary is because of the ureter not being anatomically correct within the VUJ. Secondary is due to something else, e.g. a neurogenic bladder wall

Question 2

How do we diagnosis vesicoureteric reflux?

Answer 2

Firstly, it is a clinical diagnosis based on a combination of history, clinical findings and also imaging. WRT imaging: This can be done by a few different scans. But both require injection of dye into the bladder. Which is stressful for kids. Gold standard is the voiding cystourethrogram (also known as a micturating cystourethrogram) alternative is the radionuclide cystogram (e.g. DMSA or MAG3 scan)

Question 3

What are the current guidelines about treatment of vesico-ureteric reflux?

Answer 3

Currently there is no evidence that interventions for children with VUR confer benefit. By the same token, the studies aren’t RCTs

Question 4

What are the epidemilogical features of VUR and UTI in kids? (as in, female or male)

Answer 4

VUR is more common in males UTI is more common in females.

Question 5

What is the technical difference between complicated and uncomplicated UTI?

Answer 5

Uncomplicated is basically young, non-pregnant women with nothing else going on, no functional impairment, with no fam Hx, and unrelated to sex (therefore, all men have complicated UTI)

Question 6

Which bug is associated with fimbriae that assist pathogenesis in the urinary tract? what about urease? what about K Ag (inhibits phagocytosis and complement)

Answer 6

E coli is typically associated with this. They have type 2 fimbriae, and it helps binding to uroepithelial cells E coli also have capsular acidic polysaccharise that inhibits phagocytosis and complement binding proteus have urease, and can promote struvite (magnesium ammonium phosphate) stones, which then can be permanently infected

Question 7

What are the definitions of UTI relapse? What about UTI reinfection?

Answer 7

UTI relapse is associated with recurrence of bacteriuria with same organism less than 3 weeks after treatment, providing urine was sterile during treatment (relapse suggests failure of bacteria eradication. Prophylaxis isn’t recommended - instead we have to eradicate the bug somehow) UTI reinfection is bacteriuria was eradicated by appropriate treatment followed by infection with different organism after 7 days, or re-infection with same after 3 weeks later (this is commoner and is due to reinvasion of the urinary tract. Prophylaxis is recommended - if >2 per year)

Question 8

Who should we treat with asymptomatic bacteriuria?

Answer 8

DEFINITELY: pregnant women prior to urinary tract instrumentation (such as prior to TURBT) MAYBE: it is unclear about whether to treat all stones and also in conditions where there is a risk of papillary necrosis (such as DM, analgesia nephropathy and NSAID kidney)

Question 9

How would you counsel someone starting on UTI Ab prophylaxis?

Answer 9

Firstly - should maintain high fluid intake and frequent voiding. Secondly - prophylactic antibiotics are best used at night time, as this is when protective effect of high fluid intake is lost Thirdly, we aim for 12 months of treatment, then reassess

Question 10

What is xanthogranulomatous pyelonephritis?

Answer 10

Xanthogranulomatous pyelonephritis (XGP) is a rare form of chronic pyelonephritis and represents a chronic granulomatous disease resulting in a non-functioning kidney. Most common in middle aged women. Renal mass is often palpable. Xanthogranulomatous pyelonephritis is, as the name suggests, a chronic granulomatous process believed to be the result of subacute/chronic infection inciting a chronic but incomplete immune reaction. The kidney is eventually replaced by a mass of reactive tissue, surrounding the usually present (90%) inciting staghorn calculus with associated hydronephrosis of a greater or lesser degree. Foamy (lipid laden) macrophages predominate. Inflammatory process eventually extends into perinephric tissues and even adjacent organs. Various bacteria are isolated, however the most commonly isolated species are E coli and P mirabilis. - it is associated with urease producing bacteria that go on to create struvite stones

Question 11

What are characteristics of antibiotics used to treat infected cysts?

Answer 11

This is more common in PCKD, but can happen in patients with simple cysts. The ideal thing is to get antibiotics that have good penetrance into the cyst such as quinolones

Question 12

Why do we treat asymptomatic bacteriuria in pregnancy?

Answer 12

Firstly, 50% go on to symptomatic. Secondly 25% go on to pyelo Thirdly, UTI is associated with greater risk of pre-eclampsia Also associated with low birth weight, prematurity, spont abortion

Question 13

What are the different types of renal calculi?

Answer 13

Most common is calcium oxalate, less frequently calcium phosphate. Other types 1. uric acid 2. infection - struvite 3. cysteine stones 4. others such as indinavir

Question 14

What are some characteristics of the struvite stones?

Answer 14

These form within the collecting system and often look like staghorns, leading to their name of staghorn calculus THEY ARE ASSOCIATED WITH UREASE PRODUCING BUGS. also, because they happen in this setting, the urease producers create an alkaline environment.

Question 15

What role does dietary calcium play in the formation of renal stone formation?

Answer 15

Strangely, low intestinal calcium leads to increased oxalate absorption. The increased oxalate absorption leads to increased urinary oxalate. This leads to a saturation of oxalate in the urine, leading to more stones. There is still some urinary calcium because of bony turnover. Therefore, decreased calcium intake actually leads to more oxalate stones

Question 16

What role does dietary protein have in stone formation?

Answer 16

interestingly, increased dietary protein leads to increased amino acids. This leads to acidosis, which leads to increased bone buffering, which leads to increased serum calcium, then increased urinary calcium (leading to Ca-oxalate stones)

Question 17

How do thiazides help prevent kidney stones? Why do loop diuretics increase kidney stone formation?

Answer 17

With thiazides: On the basolateral side (not the apical / lumen side) of the distal convoluted tubule, there is a sodium/calcium exchange transporter. Well, because this diuretic acts to block NaCl reabsorption, there will be a lack of sodium inside the distal tubule cells (as more NaCl is excreted with water). These cells will then tend to use this basolateral exchanger to bring in more Na. Well, that means they will have less calcium in them (and more calcium will be brought into the interstitium). The new lack of calcium inside the cell (and corrected sodium) will tend to increase calcium reabsorption from the lumen into the distal tubule cells. Therefore increasing overall calcium in the body With frusemide: The reabsorption of calcium in the loop of Henle is primarily passive, being driven by the electrochemical gradient created by NaCl transport and occurring through the paracellular pathway. As a result, inhibiting the reabsorption of NaCl leads to a parallel reduction in that of calcium, thereby increasing calcium excretion. In the past, saline plus high doses of furosemide was a mainstay of the treatment of hypercalcemia.

Question 18

Why does high dietary sodium lead to stones?

Answer 18

High dietary sodium would lead to preferential re-absorption of sodium at the Na/Cl co-transporter. Therefore, the electrochemical gradient is spent on sodium resorption, not calcium. This leads to more luminal calcium and more stones

Question 19

What is the biggest risk factor for uric acid stones

Answer 19

acidic urine is the most important risk factor. the stones occur from uric acid in the urine. Gout has high levels or uric acid, and thus conveys a 2x risk of renal stones (in men only) the uric acid must be in an acidic environment to form. so, a pH <5.5 is the most important RF

Question 20

What causes hyperoxaluria?

Answer 20

This leads to oxalate stone formation. Dietary intake, such as spinach, rhubarb, beetroot plus others enteric causes from increased intestinal absorption.

Oxalate is absorbed from the colon. It is worst with terminal ileal disease, where the inflamm leads to increased colonic permeability.

Increased enteric absorption of oxalate is also assoc with bile salt malabs… Apparently it leads to increased colonic permeability. Therefore it is associated with Crohn’s, short bowel syndrome, ileal bypass

Question 21

what role does citrate play in renal stones

Answer 21

it forms a soluble complex with calcium. diets high in animal protein leads to decreased citrate. women secrete more citrate in urine

Question 22

What type of renal stone is invisible on all forms of scanning?

Answer 22

The stones associated with the drug indinavir

Question 23

What would urinary pH tell you about possible renal stones causes. pH < 5.5 pH > 6.5 pH > 7.5

Answer 23

pH < 5.5: risk of uric acid stone pH > 6.5: suspect RTA pH > 7.5: suspect infection with urease producing bug

Question 24

What is the medical management of renal stones?

Answer 24

Question 25

What is the management of renal stones focussing on specific risk factors?

Answer 25

Question 26

What effect does urinary pH have on stone formation?

Answer 26

Urine pH has variable effects upon stone formation.

The solubility of uric acid is markedly decreased in an acidic solution so uric acid stones are more likely to form.

However, calcium phosphate becomes less soluble at pH>6; hence calcium phosphate stones are more likely to form in an alkaline urine.