Renal stones Flashcards
Describe the differences between primary and secondary ureteric reflux
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
How do we diagnosis vesicoureteric reflux?
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)
What are the current guidelines about treatment of vesico-ureteric reflux?
Currently there is no evidence that interventions for children with VUR confer benefit. By the same token, the studies aren’t RCTs
What are the epidemilogical features of VUR and UTI in kids? (as in, female or male)
VUR is more common in males UTI is more common in females.
What is the technical difference between complicated and uncomplicated UTI?
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)
Which bug is associated with fimbriae that assist pathogenesis in the urinary tract? what about urease? what about K Ag (inhibits phagocytosis and complement)
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
What are the definitions of UTI relapse? What about UTI reinfection?
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)
Who should we treat with asymptomatic bacteriuria?
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)
How would you counsel someone starting on UTI Ab prophylaxis?
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
What is xanthogranulomatous pyelonephritis?
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
What are characteristics of antibiotics used to treat infected cysts?
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
Why do we treat asymptomatic bacteriuria in pregnancy?
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
What are the different types of renal calculi?
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
What are some characteristics of the struvite stones?
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.
What role does dietary calcium play in the formation of renal stone formation?
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
What role does dietary protein have in stone formation?
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)
How do thiazides help prevent kidney stones? Why do loop diuretics increase kidney stone formation?
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.
Why does high dietary sodium lead to stones?
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
What is the biggest risk factor for uric acid stones
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
What causes hyperoxaluria?
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
what role does citrate play in renal stones
it forms a soluble complex with calcium. diets high in animal protein leads to decreased citrate. women secrete more citrate in urine
What type of renal stone is invisible on all forms of scanning?
The stones associated with the drug indinavir
What would urinary pH tell you about possible renal stones causes. pH < 5.5 pH > 6.5 pH > 7.5
pH < 5.5: risk of uric acid stone pH > 6.5: suspect RTA pH > 7.5: suspect infection with urease producing bug
What is the medical management of renal stones?
