The patient had an ultrasonography showing bilateral multiple renal stones. Further laboratory investigations are shown in table 2
|
Test |
Value |
|
Urine volume |
1.8 L |
|
24-hr urinary calcium |
390 mg/24hr (100-300 mg/24hr) |
|
24-hr urinary oxalate |
97 mg/24hr (<40 mg/24hr) |
|
24-hr urinary uric acid |
510 mg/24hr (250-750 mg/24hr) |
|
24-hr urinary citrate |
47 mg/24 hr (> 200 mg/day for males) |
|
S. Uric acid |
6.3 mg/dl |
|
Total Alkaline phosphatase |
123 U/L |
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– Labs show increased Ca & oxalate in urine, decreased citrate concentration.
– In this pt, vitamin D supplementation increases calcium absorption and reabsorption. Increased excreted oxalate in urine binds to calcium, forming calcium oxalate stone which is favored in the absence of sufficient citrate concentration- responsible for increased urine solubility-.
– This abnormal composition of urine can be reversed by decreasing urinary Ca & oxalate excretion, increase urine solubility.
Plan of management:
1-H⬆️⬆️calciurea
⬆️⬆️oxalurea
⬇️⬇️citaturea
2-All causes Ca stone formation plus hypervitaminosis VD.
3- ⬆️fluid intake
stop VD supplementation
increase citrus. decrease food containing oxalate
1- ca oxalate stone ( ca more 250 , low oxalate)
2- low oxalate diet
good hydration
thiazide 50 mg daily
1 calcium oxalate stones ( Increased oxalate, decrease urine volume and decreased citrate)
2 increase fluid intake , reduce na intake avoid oxalate rich food like
24 hrs of calcium and oxalate with low citrate level could possibly suggest calcium oxalate stones.
the mechanism could be the low citrate which inhibits the renal stone formation , vitamin d metabolites .
patient should avoid further supplement of vitamin d, avoid oxalate containing food
diuretics
1- increased urinary excretion of calcium and oxalate with decreased citrate excretion in urine
2-secondary nephrocalcinosis due to increased calcium and oxalate excretion and decreased excretion of stone inhibitors as citrate
3- thiazide diuretics , increased water intake , salt restriction , avoid oxalate rich food as tomatoes
Interpret the above laboratory investigations.
Calcium oxalate stones are the most common renal stones.Low urine volume due to inadequate fluid intake
High urinary calcium and oxalate and low urinary citrate
What is the likely mechanism leading to recurrent stone formation in this patient?
Dietary factors, high doses of vitamin D, and several metabolic disorders can increase the concentration of calcium or oxalate in urine.In this patient meight be high oxalate , low citrate and low urine volume Increased calcium oxalate supersaturation may result from low urine volume or excessive excretion of calcium or oxalate, or combinations of these factors. Hypercalciuria and hyperoxaluria can each result from interaction of genetic susceptibility and environmental triggers, in varying proportions.,Increased intestinal oxalate absorption secondary to malabsorptive disease (enteric hyperoxaluria), dietary habits (high oxalate intake coupled with low calcium intake), alteration in gut flora which may decrease oxalate degradation in the colon, The links between genetic variability and urine calcium excretion and pH
Suggest a management plan in view of the present information emphasizing the dietary prescription.
Stop any further vitamin D ,
calcium and oxalate supplements.
Increasing fluid intakeLow-sodium & protien diet
Thank you dear colleagues for your great contributions.
Here are the explanation for this part.
1. Interpret the above laboratory investigations
Calcium oxalate stones are the most common renal stones. Low urine volume secondary to inadequate water/fluid intake along with high urinary calcium and oxalate and low urinary citrate are the leading causes of calcium oxalate renal stones. Low urinary citrate is an important risk factor for stone formation because citrate is an important inhibitor of calcium oxalate and calcium phosphate stone formation.
2. What is the likely mechanism leading to recurrent stone formation in this patient?
Urinary citrate has a protective effect against formation of calcium oxalate stone, so decrease in urinary citrate has a major contributing factor beside high urinary calcium and oxalate. Vitamin D deficiency has been shown to cause inflammation and oxidative stress, so that the correlation between calcium oxalate urolithiasis and vitamin D deficiency may result from the role of vitamin D deficiency in inducing oxidative stress and inflammation in kidney tissue. Excess vitamin D, and especially its active metabolite calcitriol, increases digestive calcium absorption—as urinary calcium excretion is directly correlated with digestive calcium absorption, vitamin D metabolites could theoretically increase calciuria and promote urinary stone formation. However, vitamin D deficiency has a role in disturbance of calcium homeostasis leading to PTH mediated increased serum calcium level and hypercalciuria. Moreover, the decrease in free intestinal calcium can lead to increased absorption of dietary oxalate and enhanced oxalate excretion due to decreased binding of oxalate by calcium in the intestinal lumen. Hyperoxaluria is associated with recurrent calcium oxalate formation, because it bind easily to calcium.
3. Suggest a management plan in view of the present information emphasizing the dietary prescription.
The patient needs to stop any further vitamin D and calcium supplements. Increasing fluid intake, potassium, and phytate are usually beneficial in decreasing the risk of renal stone formation. In addition, decreasing the intake of oxalate, animal protein, sucrose, fructose, sodium, supplemental vitamin C, and supplemental calcium may reduce the risk of stones. Increasing fluid intake, spread throughout the day, will increase the urine flow rate and lower the urine solute concentration, both of which protect against stone formation. Foods that are rich in potassium, particularly fruits and vegetables, may be beneficial. Increasing intake of fruits and vegetables, regardless of 24-hour urine values, may reduce the risk of calcium oxalate stone formation, particularly in patients who self-select a diet that is low in fruits and vegetables. This benefit is primarily the result of increasing citrate excretion. Some foods contain very large amounts of oxalate and should be restricted (eg, spinach, tomatoes, mangos and potatoes). In addition, some nuts and legumes are also high in oxalate and the intake should be limited (eg, peanuts, cashews, and almonds). A low-sodium diet can enhance proximal sodium and calcium reabsorption, leading to a reduction in calcium excretion. But restricting dietary calcium intake is not generally recommended unless it is excessive (more than 1500 mg/day).
1-
Hypercalciurea
Hyperoxalurea
Hypocitaturea
2-All lead to Ca stone formation plus hypervitaminosis VD.
3- increase fluid intake
stop VD supplementation
increase citrus. decrease food containing oxalate
1.Interpret the above laboratory investigations.
High Calcium and Oxalate excretion with a low Citrate excretion
2.What is the likely mechanism leading to recurrent stone formation in this patient?
High oxalate with low citrate lead to calcium precipitation.
3.Suggest a management plan in view of the present information emphasizing the dietary prescription.
Hydration
Low salt diet
Low protein diet
stop vitamin D supplementation
treat infection
urine alkanization
1- interpretation of lab elevation of 24hr ca and oxalate with low level of citrate.
2-the most likely mechanism for recurrant stone was high oxalate and low citrate make good media for precipitation of ca oxalate.
3- management plane good hydration stop vit d supplement avoid animal protein and diet rich with oxalate and ca
Interpretation
Mechanisms
Plan
1.Interpret the above laboratory investigations.
high urinary calcium and oxalate excretion and low urinary citrate.
2.What is the likely mechanism leading to recurrent stone formation in this patient?
multiple factors, mainly vitamin -D shots causing hypercalcemia, high oxalate, and low citrate.
3.Suggest a management plan in view of the present information emphasizing the dietary prescription.
Good hydration
K-citrate
low protein and low-salt diet.
stop Vitamin -D
and avoid food containing high oxalate(eg: peanuts) .
PATIENT HAS BILATERAL KIDNEY STONE WITH HYPERCALCIURIA , HYPEROXALURIA AND HYPOCITRATURIA WHICH WILL BE THE CAUSE OF STONE FORMATION BUT BURNING SENSATION NEEDS FOR EXCLUSION OF OTHER CAUSES INFECTION AS ONE OF THE CAUSES , NEEDS FOR DIET CONTROL ( LOW OXALATE HIGH CALCIUM DIET , STILL I WILL RECOMEND NONCONTRAST CT AND UROLOGY CONSULTATION
1.hypercalciurea,hyperoxalurea,hypocitaturea
2.hypocitriturea with hypercalciuria and hyperoxaluria most probably lead to ca stone formation added to hypervitaminosis VD
3.increase fluid intake
stop VD supplementation
increase citrus in diet and decrease food containing oxalate
urology consultation
1.Hypercaciurea, hyperoxaluria, hypocitraturia
2. Low citrate which is a natural inhibitor of stone formation with hypercaciurea and hyperoxaluria which form a nidus for stone formation
3 increases fluid intake, avoid dietary Calcium restriction , analgesia low salt diet, restriction of oxalate containing diet
Supplements with citrate, vitamin B6
Consult urosurgery
The above lab results
Urinary hypercalciuria, hyperoxaluria, with hypocitraturia.
The most likely mechanism of stone formation
Stoen formation due to hypercalciuria, hyperoxaluria, and hypocitraturia (acidic urine), may be due to hyper vitamin D, which augments intestinal calcium absorption.
Management plan;
there is hypercalciuria and hyperoxalaturia and low citrate in urine with most likley calcium oxalate stone formation.Vitamin D level are high with cause more calcium absorption and subsequently hypercalcuria. Oxalate in Urin are high and they bind with calcium and together form calcium oxalate the most common origin of renal stones. Citrat binds to calcium and prevent crystall formation.More fluid intake to achieve a level of 2.5-3 l a day, increase intake of citrus fruit that are good source of citrate . He should reduce food that are high on oxalate like spinat, rhubarb, chocolate. Increase Urin PH
We have hypercalciuria, hyperoxaluria and hypocitraturia. 1.8 L of urine needs to be increased to more than 2.5 . Hypercalciuria may improve with hydration and avoidance of vitamin D. When calcium is normal, we may use thiazide to decrease calciuria. Low citrate level in urine needs to be managed with potassium citrate with paying attention to potassium levels. Avoidance of vitamin C and nutrients rich in oxalate. It is important to differentiate whether ocaluria is primary or secondary.
1. Interpret the above laboratory investigations.
2. What is the likely mechanism leading to recurrent stone formation in this patient?
3. Suggest a management plan in view of the present information emphasizing the dietary prescription.
increased fluid intake – aim for urine output >2 ls/day
Limit sodium intake
low animal protein diet
against a low calcium diet
limit intake of high oxalate foods and supplemental vit C
limit intake of sucrose and fructose
weight loss
Thiazide diuretics- lower calcium excretion.
Potassium citrate or potassium bicarbonate-increase urinary citrate excretion
high urinary calcium and oxalate excretion and low urinary citrate.
multiple factors, mainly vitamin -D shots causing hypercalcemia, high oxalate, and low citrate.
Good hydration
K-citrate
low protein and low-salt diet.
stop Vitamin -D
and avoid food containing high oxalate(eg: peanuts)
1.Interpret the above laboratory investigations
2.What is the likely mechanism leading to recurrent stone formation in this patient
3.Suggest a management plan in view of the present information emphasizing the dietary prescription.
Hypocitraturia and hyperoxaluria are the most factored which precipitate renal stones.
Suggest a management plan in view of the present information emphasizing the dietary prescription
good rehydration
stop Vit D
STRAT oral B6
high citrate through Kcitrate
low oxatlate diet
urology referral
Interpret the above laboratory investigations.
What is the likely mechanism leading to recurrent stone formation in this patient?
Suggest a management plan in view of the present information emphasizing the dietary prescription.
1- hypercalciuria and hyperoxaluria ,hypocitraturia
2-recurrent stone due to hypercalciuria and hypocitraturia amd hyperoxaluria
3-
1-stop viatmin D
2-good hydration
3-restricting foods high in oxalates, limiting salt, and decreasing animal protein and sugar (high fructose corn syrup).
4-oral K citrate
1. Interpret the above laboratory investigations.
Hypercalciuria- Hyperoxaluria
2. What is the likely mechanism leading to recurrent stone formation in this patient?
A high level of 24-hr urinary calcium is the most likely cause of the recurrent stone formation in this patient
3. Suggest a management plan in view of the present information emphasizing the dietary prescription.
Stop vit D injection
Restrict calcium and oxalate rich diet
Hydration and pyridoxine
Potassium citrateUrological consultation
the investigation revealed
hyper oxaluria and hyper calceruia
other resting investigation win normal
hyperoxaluria lead to formation of calcium oxalate crystal and multiple stone formation
Management plan
our target to lower the level of oxalate to prevent calcium oxalate crystals formation and stone formation
avoid diet rich in oxalate and calcium
vit. b6 ( pyridoxine )
oral doses of potassium citrate
drinking plenty fluids up to 2.5 – 3 l/d
Interpret the above laboratory investigations.
What is the likely mechanism leading to recurrent stone formation in this patient?
Suggest a management plan in view of the present information emphasizing the dietary prescription.