Nephrolithiasis, commonly known as kidney stones, refers to the formation of hard mineral and salt deposits within the kidneys or urinary tract. These stones can vary in size, ranging from tiny grains to larger, more substantial formations. Nephrolithiasis is a relatively common condition and can affect people of all ages, although it is more prevalent in adults.

1. Nephrolithiasis
SHISODIA HARSH VARDHAN SINGH
JONELTA FOUNDATION OF MEDICINE
18-1059-267
Block 10B

2. Index
• Introduction
• Epidemiology
• Pathogenesis
• Risk factors
• Approach to the patient

3. Introduction
• kidney stone disease
• common, painful, and costly
condition
• stone may form due to
crystallization of lithogenic factors
in the upper urinary tract
• patients who have had renal colic
report that it is the worst pain

4. • There are various types of kidney stones
Calcium oxalate stones
calcium phosphate
uric acid
struvite
cystine

5. Calcium Oxalate
is include higher urine calcium,
higher urine oxalate, and lower urine citrate.
This stone type is insensitive to pH in the
physiologic range.

6. Calcium phosphate
are more common
in patients with distal renal tubular
acidosis and primary
hyperparathyroidism, Including higher
concentrations of urine calcium and
lower concentrations of urine citrate.

7. Uric Acid
has two main risk factors for uric
acid stones are persistently low urine pH and
higher uric acid excretion. Urine pH is the
predominant influence on uric acid
solubility,Alkalinizing the urine can be readily
achieved by increasing the intake of foods
rich in alkali (e.g., fruits and vegetables) and
reducing the intake of foods that produce
acid (e.g., animal flesh).

8. Cystine
is not easily modified and long-term dietary cystine restriction
is not feasible and is unlikely to be successful.

9. Struvite
Also known as infection
stone or triple phosphate stone ,
form only when the upper urinary
tract is infected with urease
producing bacteria

10. • Infectious stones, if not appropriately treated,
can have devastat- ing consequences and lead to
end-stage renal disease.

11. Epidemiology
• Nephrolithiasis is a global disease
• NationalHealth and Nutrition
Examination Survey data
2007–2010 - 19% of men
9% of
women will develop

12. ASSOCIATED MEDICAL CONDITIONS
• systemic disorder
• Several conditions predispose to stone formation
gastrointestinal
malabsorption
primary hyperparathyroid-
ism
Obesity
Type 2 diabetes mellitus
distal renal tubular acidosis

13. • Other medical condition with a history of nephrolithiasis
Hypertension
Gout
Cholelithiasis
reduced bone mineral density
chronic kidney disease

14. Individuals with medullary
sponge kidney (MSK)
• condition designated by an anatomic description
• have metabolic abnormality
higher levels of urine
calcium
lower levels of urine
citrate

15. • As intravenous urography is now rarely used, the
diagnosis of MSK has become less frequent
• nephrolithiasis does not directly cause upper urinary
tract infections

16. Pthogenesis
• processes involved in crystal
formation
• helpful to view urine as a complex
solution
• Supersaturation
• most clinically important inhibitor
of calcium-containing stones is
urine citrate.
• supersaturation

17. • Supersaturation
calculated value
and does not perfectly predict stone formatinon
useful guide as it integrates the multiple factors that are
measured in a 24-h urine collection.

18. • Thus, the process of stone formation may begin years before a
clinically detectable stone is identified. The processes involved in
interstitial deposition are under active investigation.

19. Risk factor
• categorized as
Dietary Risk Factors
Nondietary Risk Factors
Urinary Risk Factors
Genetic Risk Factors

20. Dietary Risk Factors
• animal protein
• Oxalate
• Sodium
• Sucrose
• Fructose
• Dietary factors associated with a lower risk include calcium, potassium, and phytate.

21. Calcium
• higher dietary calcium intake is related to a
lower risk of stone formation
• Low calcium intake is contraindicated as it
increases the risk of stone formation and may
contribute to lower bone density in stone
formers.

22. OXALATE • derived from both endogenous production
and absorption of dietary oxalate.
• absorption may be higher in stone formers
• dietary oxalate is only a weak risk factor for
stone formation
• urinary oxalate is a strong risk factor for
calcium oxalate stone formation

23. OTHER
NUTRIENTS
• Vitamin C
• Higher intake of animal
protein
• Higher sodium and
sucrose intake

24. Nondietary Risk
Factors
• Age
• Race
• body size
• environment

25. Urinary Risk Factors
• low urine volume
• randomized trial has demonstrated the effectiveness of elevated fluid intake in increasing urine
volume and reducing the risk of stone recurrence.

26. URINE CALCIUM
Higher urine calcium
excretion increases the likeli- hood of
formation of calcium oxalate and calcium
phosphate stones.
URINE OXALATE
Higher urine oxalate
excretion increases the likelihood of calcium
oxalate stone formation.

27. URINE CITRATE
Urine citrate is a natural inhibitor of calcium containing
stones, lower urine citrate excretion increases the risk of stone
formation.
URINE URIC ACID
Higher urine levels of uric acid—a risk factor for uric
acid stone formation
found in individuals with excess purine
consumption and rare genetic conditions that
lead to overproduction of uric acid.

28. URINE pH
Urine pH influences the
solubility of some crystal types.
Uric acid stones when pH <5.5 or lower
calcium phosphate stones when ph >6.5
or higher
• Cystine is more soluble at higher urine
pH
Note - Calcium oxalate stones are not
influenced by urine pH.

29. Genetic Risk Factors
• The risk of Nephrolithiasis is more than
twofold greater in individuals with a family
history of stone disease
due to a combination of genetic predisposition
and similar environmental exposures
• number of monogenic disorders cause
Nephrolithiasis

30. • most common and well-characterized rare monogenic
disorders that lead to stone formation are primary
hyperoxaluria and cystinuria
Hyperoxaluria
Cystinuria

31. APPROACH TO THE
PATIENT
CLINICAL PRESENTATION
There are two common presentations for individuals with an acute
stone event: renal colic and painless gross hematuria.
Renal colic is a misnomer because pain typically does not subside completely;
rather, it varies in intensity. When a stone moves into the ureter, the
discomfort often begins with a sudden onset of unilateral flank pain.
The intensity of the pain can increase rapidly. If the stone lodges in the upper
part of the ureter, pain may radiate anteriorly; if the stone is in the lower part
of the ureter, pain can radiate to the ipsilateral testicle in men or the ipsilateral
labium in women.

32. DIAGNOSIS
• The diagnosis is often made on the basis of the
history, physical examination, and urinalysis.
Thus, it may not be necessary to wait for
radiographic confirmation before treating the
symptoms. The diagnosis is confirmed by an
appropriate imaging study—prefer- ably
helical CT, which is highly sensitive, allows
visualization of uric acid stones
• History and physical examination
• Helical computed tomography (CT)
• Abdominal ultrasound
• Renal ultrasound

33. Other
Diagnosis
maybe
confused
• Other diagnoses may be confused with acute
renal colic. If the stone is lodged at the right
ureteral pelvic junction, symptoms may mimic
those of acute cholecystitis
• If the stone blocks the ureter as it crosses over
the right pelvic brim, symptoms may mimic
acute appendicitis, whereas blockage at the left
pelvic brim may be confused with acute
diverticulitis
• Acute renal colic
• Acute appendicitis
• Acute pyelonephritis

34. LABORATORY
EVALUATION
• The following serum levels should be determined:
• Electrolytes (to uncover hypokalemia or renal
tubular acidosis)
• Creatinine
• Calcium
• Uric acid
• PTH level should be measure if indicated by high-
normal or elevated serum and urine calcium
concentrations.
• Examination of the sediment
• 24-h urine collections

35. LONG-TERM FOLLOW-UP
• The preventive regimens described above do not cure the underlying pathophysiologic
process. Thus these recommendations typically need to be followed for the patient’s
lifetime, and it is essential to tailor recommendations in a way that is acceptable to the
patient. Because the memory of the acute stone event fades and patients often return to
old habits (e.g., insufficient fluid intake), long-term follow-up, including repeat 24-h urine
collections, is important to ensure that the preventive regimen has been implemented and
has has resulted in the desired reduction in the risk of new stone formation.

36. PREVENTION OF
NEW STONE
FORMATION
• Recommendations for preventing stone formation
depend on the stone type and the results of
metabolic evaluation.
• After remediable secondary causes of stone
formation (e.g., primary hyperparathyroidism) are
excluded, the focus should turn to modification of
the urine composition to reduce the risk of new
stone formation.
• For all stone types, consistently diluted urine reduces
the likelihood of crystal formation. The urine volume
should be at least 2 L/d.