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RENAL CALCULI
OUTLINE OF THE CONTENT 
DEFINITION OF RENAL CALCULI 
INCIDENCE OF RENAL CALCULI 
RISK FACTORS FOR RENAL CALCULI 
CLASSIFICATION OF RENAL CALCULI 
ETIOLOGY : PATHOPHYSIOLOGY 
SITES OF IMPACTION
OUTLINE OF THE CONTENT 
• SIGNS AND SYMPTOMS OF RENAL 
CALCULI 
• COMPLICATIONS OF RENAL CALCULI 
• DIAGNOSIS OF RENAL CALCULI 
• MANAGEMENT OF RENAL CALCULI 
• VEDIO ON ESWL
INTRODUCTION 
Kidney stones (called renal calculi (from 
Latin renes, "kidney" and calculi, "pebbles") 
are solid concretions or crystal aggregations 
formed in the kidneys from dietary minerals.
DEFINITION OF RENAL CALCULI 
Renal calculi a condition in which there is a 
formation of stones within the renal system 
that is kidney, urethra and bladder.
INCIDENCE OF RENAL CALCULI 
 Kidney stones are a significant source of 
morbidity with an annual incidence of 1–2 per 
1000 and a lifetime prevalence of 3–5%. 
 80% of those with kidney stones are men; 
most stones in women are due to either 
metabolic defects (such as cystinuria) or 
infection.
INCIDENCE OF RENAL CALCULI CONT... 
 Recurrence rates are estimated at 50% over a 
10 year period and 75% over 20 years, with 
some experiencing ten or more episodes over 
the course of a lifetime. 
 The incidence of urolithiasis increases to 20- 
25% in the Middle East, partly due to the 
increased risk of dehydration in hot climates.
INCIDENCE OF RENAL CALCULI CONT... 
Men most commonly experience their first 
episode between age 30- 40 years, while for 
women the age at first presentation is 
somewhat later.
RISK FACTORS OF RENAL CALCULI 
 Occupation 
 Family history (cystinuria inherited metabolic 
disorder) 
 Dietary pattern of family diet high in 
calcium, vitaminD, milk, protein, oxalate, 
alkali. 
 Dehydration 
 Small bowel disease : Krohn’s disease 
 Medical conditions: Hypercalcuria 
Hyperparathyrodism, and Gout
RISK FACTORS OF RENAL CALCULI CONT… 
 Urinary tract infection 
 Urinary stasis 
 Immobility 
 Urinary tract obstruction 
 Hypercalcemia
CLASSIFICATION OF RENAL CALCULI 
Kidney stones are typically classified by their 
1. Location 
2. Chemical composition
CLASSIFICATION OF RENAL CALCULI… 
1. Location 
Urolithiasis 
Nephrolithiasis 
Calyceal 
ureterolithiasis 
cystolithiasis.
CLASSIFICATION OF RENAL CALCULI… 
Urolithiasis refers to stones originating 
anywhere in the urinary system, including the 
kidneys and bladder. 
Nephrolithiasis refers to the presence of such 
calculi in the kidneys.
CLASSIFICATION OF RENAL CALCULI… 
Calyceal calculi refers to aggregations in 
either the minor or major calyx, parts of the 
kidney which pass urine into the ureter. 
The condition is called ureterolithiasis when a 
calculus or calculi are located in the ureter. 
Stones may also form or pass into the bladder, 
condition referred to as cystolithiasis.
CLASSIFICATION OF RENAL CALCULI… 
2. Chemical composition 
Calcium-containing stones 
Struvite stones 
Uric acid stones
CLASSIFICATION OF RENAL CALCULI… 
2. Chemical composition 
Calcium-containing stones 
Calcium-containing stones represent about 
80% of cases. 
These typically contain calcium oxalate either 
alone or in combination with calcium 
phosphate 
The formation of calcium phosphate stones is 
associated with conditions such as 
hyperparathyroidism and renal tubular acidosis
CLASSIFICATION OF RENAL CALCULI… 
Struvite stones 
• 10-15% of urinary calculi are composed of 
struvite (ammonium magnesium phosphate). 
• Struvite stones (also known as "infection 
stones“ “Staghorn stone”, urease or triple-phosphate 
stones), form most often in the 
presence of infection by urea-splitting bacteria.
CLASSIFICATION OF RENAL CALCULI… 
Struvite stones cont….. 
The enzyme urease, these organisms metabolize 
urea into ammonia and carbon dioxide. 
This alkalinizes the urine, resulting in favorable 
conditions for the formation of struvite stones. 
 Proteus vulgaris 
 Klebsiella, 
 Enterobacter 
 Ureaplasma urealyticum are the most common 
organisms
CLASSIFICATION OF RENAL CALCULI… 
Struvite stones cont….. 
These infection stones are commonly observed in 
people who have factors which predispose them 
to urinary tract infections, such as those with 
spinal cord injury and other forms of neurogenic 
bladder, ileal conduit urinar diversion, 
vesicoureteral reflux, and obstructive uropathies.
CLASSIFICATION OF RENAL CALCULI… 
Uric acid stones 
About 5-10% of all stones are formed from uric 
acid. 
Uric acid stones may form in association with 
conditions that cause hyperuricosuria (an 
excessive amount of uric acid in the urine) with 
or without high hyperuricemia (an excessive 
amount of uric acid in the serum)
CLASSIFICATION OF RENAL CALCULI… 
Uric acid stones cont….. 
People afflicted with xanthinuria often produce 
stones composed of xanthine 
People with certain rare inborn errors of 
metabolism have a propensity to accumulate 
crystal-forming substances in their urine. For 
example, those with cystinuriaform stones 
composed of cystine
ETIOLOGY : PATHOPHYSIOLOGY 
Supersaturation of urine 
Inhibitors of stone formation 
Calcium 
others
ETIOLOGY : PATHOPHYSIOLOGY 
Supersaturation of urine 
When the urine becomes supersaturated (when 
the urine solvent contains more solutes than it 
can hold in solution) with one or more crystal-forming 
substances, 
a seed crystal may form through the process of 
nucleation.
Heterogeneous nucleation (where there is a 
solid surface present on which a crystal can 
grow) proceeds more rapidly than 
homogeneous nucleation (where a crystal must 
grow in liquid medium with no such surface), 
because it requires less energy. 
Adhering to cells on the surface of a renal 
papillae, a seed crystal can grow and aggregate 
into an organized mass.
• Depending on the chemical composition of the 
crystal, the stone-forming process may proceed 
more rapidly when the urine pH is unusually 
high or low.
ETIOLOGY : PATHOPHYSIOLOGY CONT. 
Inhibitors of stone formation 
Normal urine contains chelating agents such as 
citrate that inhibit the nucleation, growth, and 
aggregation of calcium-containing crystals.
ETIOLOGY : PATHOPHYSIOLOGY CONT. 
Inhibitors of stone formation: 
Other endogenous inhibitors include 
calgranulin(an S-100 calcium binding protein), 
nephrocalcin (an acidic glycoprotein), 
prothrombin F1 peptide, and bikunin (uronic 
acid-rich protein). 
 When these substances fall below their normal 
proportions, stones can form out of an 
aggregation of crystals.
ETIOLOGY : PATHOPHYSIOLOGY CONT. 
Calcium 
People who take supplemental calcium have a 
higher risk of developing kidney stones 
In the Women's Health Initiative, 
postmenopausal women who consumed 
1,000 milligrams of supplemental calcium and 
400 IU of vitamin D per day for 7 years had a 
17% higher risk of developing kidney stones 
than subjects taking a placebo.
ETIOLOGY : PATHOPHYSIOLOGY CONT. 
Calcium 
This is perhaps related to the role of calcium in 
binding ingested oxalate in the gastrointestinal 
tract. 
Unlike supplemental calcium, high intakes of 
dietary calcium do not appear to cause kidney 
stones and may actually protect against their 
development
ETIOLOGY : PATHOPHYSIOLOGY CONT. 
Role of dietary animal protein 
Animal protein than the body needs, and as the 
excess amino acids are broken down and 
excreted, the sulfurous amino acids (typically 
derived from animal rather than vegetarian 
foods) cause calcium to be excreted in the 
urine.
ETIOLOGY : PATHOPHYSIOLOGY CONT. 
• Red meat also contains acids that need to be 
excreted and this acidity constitutes another 
risk factor for kidney stones 
• High intake of animal protein also presents a 
greater uric acid load to be excreted by the 
kidney. This in turn acidifies the urine, 
increasing the risk of uric acid stones.
ETIOLOGY : PATHOPHYSIOLOGY CONT. 
Other 
Water fluoridation may increase the risk of 
kidney stone formation. 
Ingestion of vitamin C supplements is 
associated with an increased incidence of 
kidney stones.
ETIOLOGY : PATHOPHYSIOLOGY CONT. 
Other 
Alcohol consumption, binge drinking can lead 
to systemic dehydration, which can in turn lead 
to the development of kidney stones. 
Astronauts seem to show a higher risk of 
developing kidney stones during or after space 
flights of long duration.
UROLITHIASIS – SITES OF IMPACTION
SIGNS AND SYMPTOMS OF RENAL CALCULI 
Obstruction of urine flow through one or both 
ureters. 
Oliguria (reduced urinary volume) caused by 
obstruction of the bladder or urethra by a stone or 
rarely, simultaneous obstruction of both ureters by 
two separate stones. 
Postrenal azotemia and 
Hydronephrosis (distension and dilation of the 
renal pelvis and calyces
SIGNS AND SYMPTOMS OF RENAL CALCULI… 
Flank pain 
Costovertebral 
tenderness 
Cool, moist skin 
Pallor, 
Diaphoresis 
Diagram showing the typical 
location of renal colic, from below 
the rib cage to just above the pelvis
SIGNS AND SYMPTOMS OF RENAL CALCULI… 
Frequency and urgency in urination 
dysuria, 
Chills and fever 
Hematuria 
Nausea and vomiting
SIGNS AND SYMPTOMS OF RENAL CALCULI… 
• Hallmark symptoms of 
kidney stones include 
renal colic, fever, 
blood, pus in the urine, 
and painful urination. 
• Pain, most commonly 
felt in the flank, lower 
abdomen and groin (a 
condition called renal 
colic.
SIGNS AND SYMPTOMS OF RENAL CALCULI… 
Renal colic, which typically comes in waves 
lasting 20 to 60 minutes, is caused by peristaltic 
contractions of the ureter as it attempts to expel 
the stone. 
It typically begins in the flank or lower back, 
often radiating to the groin or in men, to the 
testes. 
Renal colic can be associated with nausea and 
vomiting.
COMPLICATIONS OF RENAL CALCULI 
 Chronic Urinary Tract Infection 
 RENAL OBSTRUCTION 
 UTERO-VESICAL REFLUX 
 HYDRO NEPHROSIS 
 PYELO NEPHROSIS 
 Acute Renal Failure 
 Chronic Renal Failure
DIAGNOSIS OF RENAL CALCULI 
Diagnosis of kidney stones is made on the basis 
of information obtained from the 
History, 
Physical examination, 
Urinalysis, and 
Radiographic studies
DIAGNOSIS OF RENAL CALCULI… 
History and physical examination 
Clinical diagnosis is usually made on the basis of 
the location and severity of the pain, which is 
typically colicky in nature (comes and goes in 
spasmodic waves). 
Physical examination may reveal fever and 
tenderness at the costovertebral angle on the 
affected side.
DIAGNOSIS OF RENAL CALCULI… 
 Urinalysis 
Provides excellent information about renal function and 
condition relative to fluids and Electrolytes 
 Urinalysis – know normal (color, odor, consistency & 
related teaching) 
 Clean catch – know teaching of method and purpose 
 Culture and Sensitivity – know teaching 
 Urine chemistry pyuria, proteinuria, hematuria, and 
wbc’s count.
DIAGNOSIS OF RENAL CALCULI… 
Urinalysis 
pH: Indicates acidity or alkalinity 
 Normal range 4.5-8.0 
 Normal for urine 6.0 (acid) 
Osmolality 
 pinpoints fluid balance 
 normal = 300-1200 mOsm/kg 
 example: as urine Osm. increases. urine 
volume decreases (urine more concentrated)
DIAGNOSIS OF RENAL CALCULI… 
Electrolytes 
Not frequently measured 
Requires 24-hour specimen 
Changes in urinary electrolytes highly 
suggestive of renal impairment 
Sodium extremely suggestive of type of acute 
renal failure 
<20 mEq/L = pre-renal 
Normal or high >20 mEq/L
DIAGNOSIS OF RENAL CALCULI… 
Creatinine Clearance test 
A direct measurement of glomerular 
filtration rate 
Best indicator of overall kidney function 
Clearance expressed in ml/min 
 Normal: male 90-139mL/min 
female 80-125mL/min 
Measured by completing a 24 hr urine with 
corresponding blood test.
DIAGNOSIS OF RENAL CALCULI… 
Serum Creatinine 
 By-product of muscle metabolism 
 Appears in serum in amts. proportional to body 
muscle mass 
 Fluctuates little – excreted entirely by kidneys 
 Normal about 0.7-1.5 mg/dL 
• ↓ elderly and with low muscle mass 
• Creatinine: >1.5 (>50% loss), >4.8 (75% loss) 
and >10 (90% loss)
DIAGNOSIS OF RENAL CALCULI… 
• BUN/Creatinine Ratio 
Normal ratio = between 6:1 to 20:1 
When both BUN and [Cr] levels increase at same 
rate (ratio remains normal) – suggestive of renal 
dysfunction 
When BUN rises faster then [Cr] (ratio increased) 
suggestive of dehydration, hypo perfusion, 
protein catabolism, GI bleeds
DIAGNOSTICS: KUB 
KUB (kidney, ureters, 
bladder) 
No preparation 
No contrast 
Shows: 
• Stones 
• Strictures 
• Calcifications 
• Obstructions
DIAGNOSTICS: INTRAVENOUS PYELOGRAM 
IVP/ IVU 
 Series of x-ray after 
dye injection 
 To measure size, 
shape, etc of kidneys 
 Detect obstructions 
 Assess for masses 
Client preparation and 
teaching important 
nursing function
DIAGNOSTICS: RENAL ARTERIOGRAM 
Angiogram 
 Inject contrast into 
renal artery via 
femoral catheter 
 Visualize renal 
vascular 
abnormalities 
 Same prep as IVP 
 Monitor for bleeding 
after procedure
DIAGNOSTICS: MRI: ARTERIAL 
 New and thought to 
be more useful than 
other artery/venous 
grams 
 Very expensive
DIAGNOSTICS: CYSTOGRAM 
Cystogram 
 Contrast into 
bladder 
 Evaluate bladder 
and vesicoureteral 
reflux
DIAGNOSTICS: RETROGRADE PYELOGRAM 
RETROGRADE 
PYELOGRAM 
 x-ray after contrast 
into kidneys. 
 Done by 
cystoscope and 
urethral catheters 
placed into renal 
pelvis
DIAGNOSTICS OF RENAL CALCULI 
• Ultrasound – differentiates between fluid and 
mass, notes obstructions (no dye) 
• Cystoscopy – direct visualization of bladder, can 
be used for diagnosis or treatment (no dye) 
• Biopsy – used for definitive diagnosis (no dye)
MANAGEMENT OF RENAL CALCULI 
• Medical management 
• Surgical management 
• Nursing management
MANAGEMENT OF RENAL CALCULI 
Medical management 
• 85% of the time, it is possible to spontaneously 
pass a kidney stone with urination 
• Stones larger than 6 millimeters will almost 
always require some form of intervention, 
however. 
• Assuming there is no high-grade obstruction or 
associated infection in the urinary tract, and 
symptoms are relatively mild, various non-surgical 
measures can be used to encourage the 
passage of a stone.
MANAGEMENT OF RENAL CALCULI… 
Analgesia 
 requires intravenous administration of NSAIDs 
or opioids in an emergency department setting. 
 Intravenous acetaminophen appears to be 
effective.
MANAGEMENT OF RENAL CALCULI… 
Alpha adrenergic blockers 
 as tamsulosin (Flomax) may increase the 
spontaneous passage of the stone by 30%.
MANAGEMENT OF RENAL CALCULI… 
Diuretics (dietary and medicinal) 
 One of the recognized medical therapies for 
prevention of stones is the thiazide diuretics. 
 Thiazides inhibit the formation of calcium-containing 
stones by reducing urinary calcium 
excretion, an effect independent of their 
diuretic properties.
MANAGEMENT OF RENAL CALCULI… 
Urine alkalinization 
 The mainstay for medical management of uric 
acid stones is alkalinization (increasing the 
pH) of the urine. Uric acid stones are among 
the few types amenable to dissolution therapy, 
referred to as chemolysis. 
 Acetazolamide (Diamox) is a medication that 
alkalinizes the urine.
MANAGEMENT OF RENAL CALCULI… 
Allopurinol 
 For people with hyperuricosuria and calcium 
stones, Allopurinol (Zyloprim) is one of the 
few treatments.
MANAGEMENT OF RENAL CALCULI… 
 Allopurinol interferes with the production of 
uric acid in the liver. 
 The drug is also used in patients with gout or 
hyperuricemia (high serum uric acid levels). 
 Dosage is adjusted to maintain a reduced 
urinary excretion of uric acid. 
 Serum uric acid level at or below 
6 milligrams/100 mL) is often a therapeutic 
goal for patients with gout or hyperuricemia.
MANAGEMENT OF RENAL CALCULI… 
 Diet 
 for the calcium stones ( acid ash with limited 
intake of calcium and milk products 
 for oxalates stones ( alkaline ash with 
limited intake of foods high in oxalates 
 for uric acid stones ( alkaline ash with 
limited intake of foods high in purine 
 A high fluid of 3000ml per day after episode 
of urolithiasis to produce urine output of 2L 
per day 
 Intravenous therapy (fluid replacement ) 
 Activity as tolerated
MANAGEMENT OF RENAL CALCULI… 
Surgical management 
Invasive management 
Non invasive managements
MANAGEMENT OF RENAL CALCULI… 
Surgical management 
Non invasive managements 
 Electro hydraulic lithotripsy 
 Ultrasonic lithotripsy 
 Laser impulse (holmium laser) 
 Extra corporeal shock wave lithotripsy
MANAGEMENT OF RENAL CALCULI… 
 Electro hydraulic lithotripsy
MANAGEMENT OF RENAL CALCULI… 
 Ultrasonic lithotripsy 
 Laser impulse 
 Extra corporeal shock wave lithotripsy 
Extracorporeal shock wave lithotripsy (ESWL) 
involves the use of a lithotriptor machine to 
deliver externally-applied, focused, high-intensity 
pulses of ultrasonic energy to cause 
fragmentation of a stone over a period of 
around 30–60 minutes.
MANAGEMENT OF RENAL CALCULI… 
Surgical management 
Invasive managements 
 Percutaneous nephrostolithotomy 
 Cystolithophaxy 
 Pyelolithotomy (incision into renal pelvis) 
 Cystotomy(bladder calculi) 
 Nephrotomy 
 Ureteroscopic surgery
MANAGEMENT OF RENAL CALCULI… 
Nursing management 
 Maintain proper nutrition 
 Force fluids 3 Liter / day 
 Assess renal status 
 Monitor and record vital signs, urine output, 
input and output, daily weight, specific gravity, 
lab studies, and urine pH. 
 Administer medication as prescribed 
 Allay the patient anxiety
MANAGEMENT OF RENAL CALCULI… 
 Continue straining urine and giving warm baths 
and warm soaks to flanks to reduce pain 
Instruct on home care 
Increase fluid intake during hot 
Weather, illness, and exercise 
Void when urge is felt 
Test urine PH 
Increase fluid at night and void frequently
NURSING DIAGNOSIS 
• Acute pain related to irritation of stone and 
inadequate pain control or comfort as 
manifested by complaints of pain, facial 
grimicing, restlessness. 
• Ineffective therapeutic regimen management 
related to lack of knowledge about 
prevention, recurrence, diet, fluid 
requirement as manifested by questions that 
indicate lack of knowledge.
Renal calculli Veeresh VG RN
Renal calculli Veeresh VG RN
Renal calculli Veeresh VG RN

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Renal calculli Veeresh VG RN

  • 1.
  • 3. OUTLINE OF THE CONTENT DEFINITION OF RENAL CALCULI INCIDENCE OF RENAL CALCULI RISK FACTORS FOR RENAL CALCULI CLASSIFICATION OF RENAL CALCULI ETIOLOGY : PATHOPHYSIOLOGY SITES OF IMPACTION
  • 4. OUTLINE OF THE CONTENT • SIGNS AND SYMPTOMS OF RENAL CALCULI • COMPLICATIONS OF RENAL CALCULI • DIAGNOSIS OF RENAL CALCULI • MANAGEMENT OF RENAL CALCULI • VEDIO ON ESWL
  • 5. INTRODUCTION Kidney stones (called renal calculi (from Latin renes, "kidney" and calculi, "pebbles") are solid concretions or crystal aggregations formed in the kidneys from dietary minerals.
  • 6. DEFINITION OF RENAL CALCULI Renal calculi a condition in which there is a formation of stones within the renal system that is kidney, urethra and bladder.
  • 7. INCIDENCE OF RENAL CALCULI  Kidney stones are a significant source of morbidity with an annual incidence of 1–2 per 1000 and a lifetime prevalence of 3–5%.  80% of those with kidney stones are men; most stones in women are due to either metabolic defects (such as cystinuria) or infection.
  • 8. INCIDENCE OF RENAL CALCULI CONT...  Recurrence rates are estimated at 50% over a 10 year period and 75% over 20 years, with some experiencing ten or more episodes over the course of a lifetime.  The incidence of urolithiasis increases to 20- 25% in the Middle East, partly due to the increased risk of dehydration in hot climates.
  • 9. INCIDENCE OF RENAL CALCULI CONT... Men most commonly experience their first episode between age 30- 40 years, while for women the age at first presentation is somewhat later.
  • 10. RISK FACTORS OF RENAL CALCULI  Occupation  Family history (cystinuria inherited metabolic disorder)  Dietary pattern of family diet high in calcium, vitaminD, milk, protein, oxalate, alkali.  Dehydration  Small bowel disease : Krohn’s disease  Medical conditions: Hypercalcuria Hyperparathyrodism, and Gout
  • 11. RISK FACTORS OF RENAL CALCULI CONT…  Urinary tract infection  Urinary stasis  Immobility  Urinary tract obstruction  Hypercalcemia
  • 12. CLASSIFICATION OF RENAL CALCULI Kidney stones are typically classified by their 1. Location 2. Chemical composition
  • 13. CLASSIFICATION OF RENAL CALCULI… 1. Location Urolithiasis Nephrolithiasis Calyceal ureterolithiasis cystolithiasis.
  • 14. CLASSIFICATION OF RENAL CALCULI… Urolithiasis refers to stones originating anywhere in the urinary system, including the kidneys and bladder. Nephrolithiasis refers to the presence of such calculi in the kidneys.
  • 15. CLASSIFICATION OF RENAL CALCULI… Calyceal calculi refers to aggregations in either the minor or major calyx, parts of the kidney which pass urine into the ureter. The condition is called ureterolithiasis when a calculus or calculi are located in the ureter. Stones may also form or pass into the bladder, condition referred to as cystolithiasis.
  • 16. CLASSIFICATION OF RENAL CALCULI… 2. Chemical composition Calcium-containing stones Struvite stones Uric acid stones
  • 17. CLASSIFICATION OF RENAL CALCULI… 2. Chemical composition Calcium-containing stones Calcium-containing stones represent about 80% of cases. These typically contain calcium oxalate either alone or in combination with calcium phosphate The formation of calcium phosphate stones is associated with conditions such as hyperparathyroidism and renal tubular acidosis
  • 18. CLASSIFICATION OF RENAL CALCULI… Struvite stones • 10-15% of urinary calculi are composed of struvite (ammonium magnesium phosphate). • Struvite stones (also known as "infection stones“ “Staghorn stone”, urease or triple-phosphate stones), form most often in the presence of infection by urea-splitting bacteria.
  • 19. CLASSIFICATION OF RENAL CALCULI… Struvite stones cont….. The enzyme urease, these organisms metabolize urea into ammonia and carbon dioxide. This alkalinizes the urine, resulting in favorable conditions for the formation of struvite stones.  Proteus vulgaris  Klebsiella,  Enterobacter  Ureaplasma urealyticum are the most common organisms
  • 20. CLASSIFICATION OF RENAL CALCULI… Struvite stones cont….. These infection stones are commonly observed in people who have factors which predispose them to urinary tract infections, such as those with spinal cord injury and other forms of neurogenic bladder, ileal conduit urinar diversion, vesicoureteral reflux, and obstructive uropathies.
  • 21. CLASSIFICATION OF RENAL CALCULI… Uric acid stones About 5-10% of all stones are formed from uric acid. Uric acid stones may form in association with conditions that cause hyperuricosuria (an excessive amount of uric acid in the urine) with or without high hyperuricemia (an excessive amount of uric acid in the serum)
  • 22. CLASSIFICATION OF RENAL CALCULI… Uric acid stones cont….. People afflicted with xanthinuria often produce stones composed of xanthine People with certain rare inborn errors of metabolism have a propensity to accumulate crystal-forming substances in their urine. For example, those with cystinuriaform stones composed of cystine
  • 23. ETIOLOGY : PATHOPHYSIOLOGY Supersaturation of urine Inhibitors of stone formation Calcium others
  • 24. ETIOLOGY : PATHOPHYSIOLOGY Supersaturation of urine When the urine becomes supersaturated (when the urine solvent contains more solutes than it can hold in solution) with one or more crystal-forming substances, a seed crystal may form through the process of nucleation.
  • 25. Heterogeneous nucleation (where there is a solid surface present on which a crystal can grow) proceeds more rapidly than homogeneous nucleation (where a crystal must grow in liquid medium with no such surface), because it requires less energy. Adhering to cells on the surface of a renal papillae, a seed crystal can grow and aggregate into an organized mass.
  • 26. • Depending on the chemical composition of the crystal, the stone-forming process may proceed more rapidly when the urine pH is unusually high or low.
  • 27. ETIOLOGY : PATHOPHYSIOLOGY CONT. Inhibitors of stone formation Normal urine contains chelating agents such as citrate that inhibit the nucleation, growth, and aggregation of calcium-containing crystals.
  • 28. ETIOLOGY : PATHOPHYSIOLOGY CONT. Inhibitors of stone formation: Other endogenous inhibitors include calgranulin(an S-100 calcium binding protein), nephrocalcin (an acidic glycoprotein), prothrombin F1 peptide, and bikunin (uronic acid-rich protein).  When these substances fall below their normal proportions, stones can form out of an aggregation of crystals.
  • 29. ETIOLOGY : PATHOPHYSIOLOGY CONT. Calcium People who take supplemental calcium have a higher risk of developing kidney stones In the Women's Health Initiative, postmenopausal women who consumed 1,000 milligrams of supplemental calcium and 400 IU of vitamin D per day for 7 years had a 17% higher risk of developing kidney stones than subjects taking a placebo.
  • 30. ETIOLOGY : PATHOPHYSIOLOGY CONT. Calcium This is perhaps related to the role of calcium in binding ingested oxalate in the gastrointestinal tract. Unlike supplemental calcium, high intakes of dietary calcium do not appear to cause kidney stones and may actually protect against their development
  • 31. ETIOLOGY : PATHOPHYSIOLOGY CONT. Role of dietary animal protein Animal protein than the body needs, and as the excess amino acids are broken down and excreted, the sulfurous amino acids (typically derived from animal rather than vegetarian foods) cause calcium to be excreted in the urine.
  • 32. ETIOLOGY : PATHOPHYSIOLOGY CONT. • Red meat also contains acids that need to be excreted and this acidity constitutes another risk factor for kidney stones • High intake of animal protein also presents a greater uric acid load to be excreted by the kidney. This in turn acidifies the urine, increasing the risk of uric acid stones.
  • 33. ETIOLOGY : PATHOPHYSIOLOGY CONT. Other Water fluoridation may increase the risk of kidney stone formation. Ingestion of vitamin C supplements is associated with an increased incidence of kidney stones.
  • 34. ETIOLOGY : PATHOPHYSIOLOGY CONT. Other Alcohol consumption, binge drinking can lead to systemic dehydration, which can in turn lead to the development of kidney stones. Astronauts seem to show a higher risk of developing kidney stones during or after space flights of long duration.
  • 35. UROLITHIASIS – SITES OF IMPACTION
  • 36. SIGNS AND SYMPTOMS OF RENAL CALCULI Obstruction of urine flow through one or both ureters. Oliguria (reduced urinary volume) caused by obstruction of the bladder or urethra by a stone or rarely, simultaneous obstruction of both ureters by two separate stones. Postrenal azotemia and Hydronephrosis (distension and dilation of the renal pelvis and calyces
  • 37. SIGNS AND SYMPTOMS OF RENAL CALCULI… Flank pain Costovertebral tenderness Cool, moist skin Pallor, Diaphoresis Diagram showing the typical location of renal colic, from below the rib cage to just above the pelvis
  • 38. SIGNS AND SYMPTOMS OF RENAL CALCULI… Frequency and urgency in urination dysuria, Chills and fever Hematuria Nausea and vomiting
  • 39. SIGNS AND SYMPTOMS OF RENAL CALCULI… • Hallmark symptoms of kidney stones include renal colic, fever, blood, pus in the urine, and painful urination. • Pain, most commonly felt in the flank, lower abdomen and groin (a condition called renal colic.
  • 40. SIGNS AND SYMPTOMS OF RENAL CALCULI… Renal colic, which typically comes in waves lasting 20 to 60 minutes, is caused by peristaltic contractions of the ureter as it attempts to expel the stone. It typically begins in the flank or lower back, often radiating to the groin or in men, to the testes. Renal colic can be associated with nausea and vomiting.
  • 41. COMPLICATIONS OF RENAL CALCULI  Chronic Urinary Tract Infection  RENAL OBSTRUCTION  UTERO-VESICAL REFLUX  HYDRO NEPHROSIS  PYELO NEPHROSIS  Acute Renal Failure  Chronic Renal Failure
  • 42. DIAGNOSIS OF RENAL CALCULI Diagnosis of kidney stones is made on the basis of information obtained from the History, Physical examination, Urinalysis, and Radiographic studies
  • 43. DIAGNOSIS OF RENAL CALCULI… History and physical examination Clinical diagnosis is usually made on the basis of the location and severity of the pain, which is typically colicky in nature (comes and goes in spasmodic waves). Physical examination may reveal fever and tenderness at the costovertebral angle on the affected side.
  • 44. DIAGNOSIS OF RENAL CALCULI…  Urinalysis Provides excellent information about renal function and condition relative to fluids and Electrolytes  Urinalysis – know normal (color, odor, consistency & related teaching)  Clean catch – know teaching of method and purpose  Culture and Sensitivity – know teaching  Urine chemistry pyuria, proteinuria, hematuria, and wbc’s count.
  • 45. DIAGNOSIS OF RENAL CALCULI… Urinalysis pH: Indicates acidity or alkalinity  Normal range 4.5-8.0  Normal for urine 6.0 (acid) Osmolality  pinpoints fluid balance  normal = 300-1200 mOsm/kg  example: as urine Osm. increases. urine volume decreases (urine more concentrated)
  • 46. DIAGNOSIS OF RENAL CALCULI… Electrolytes Not frequently measured Requires 24-hour specimen Changes in urinary electrolytes highly suggestive of renal impairment Sodium extremely suggestive of type of acute renal failure <20 mEq/L = pre-renal Normal or high >20 mEq/L
  • 47. DIAGNOSIS OF RENAL CALCULI… Creatinine Clearance test A direct measurement of glomerular filtration rate Best indicator of overall kidney function Clearance expressed in ml/min  Normal: male 90-139mL/min female 80-125mL/min Measured by completing a 24 hr urine with corresponding blood test.
  • 48. DIAGNOSIS OF RENAL CALCULI… Serum Creatinine  By-product of muscle metabolism  Appears in serum in amts. proportional to body muscle mass  Fluctuates little – excreted entirely by kidneys  Normal about 0.7-1.5 mg/dL • ↓ elderly and with low muscle mass • Creatinine: >1.5 (>50% loss), >4.8 (75% loss) and >10 (90% loss)
  • 49. DIAGNOSIS OF RENAL CALCULI… • BUN/Creatinine Ratio Normal ratio = between 6:1 to 20:1 When both BUN and [Cr] levels increase at same rate (ratio remains normal) – suggestive of renal dysfunction When BUN rises faster then [Cr] (ratio increased) suggestive of dehydration, hypo perfusion, protein catabolism, GI bleeds
  • 50. DIAGNOSTICS: KUB KUB (kidney, ureters, bladder) No preparation No contrast Shows: • Stones • Strictures • Calcifications • Obstructions
  • 51. DIAGNOSTICS: INTRAVENOUS PYELOGRAM IVP/ IVU  Series of x-ray after dye injection  To measure size, shape, etc of kidneys  Detect obstructions  Assess for masses Client preparation and teaching important nursing function
  • 52. DIAGNOSTICS: RENAL ARTERIOGRAM Angiogram  Inject contrast into renal artery via femoral catheter  Visualize renal vascular abnormalities  Same prep as IVP  Monitor for bleeding after procedure
  • 53. DIAGNOSTICS: MRI: ARTERIAL  New and thought to be more useful than other artery/venous grams  Very expensive
  • 54. DIAGNOSTICS: CYSTOGRAM Cystogram  Contrast into bladder  Evaluate bladder and vesicoureteral reflux
  • 55. DIAGNOSTICS: RETROGRADE PYELOGRAM RETROGRADE PYELOGRAM  x-ray after contrast into kidneys.  Done by cystoscope and urethral catheters placed into renal pelvis
  • 56. DIAGNOSTICS OF RENAL CALCULI • Ultrasound – differentiates between fluid and mass, notes obstructions (no dye) • Cystoscopy – direct visualization of bladder, can be used for diagnosis or treatment (no dye) • Biopsy – used for definitive diagnosis (no dye)
  • 57. MANAGEMENT OF RENAL CALCULI • Medical management • Surgical management • Nursing management
  • 58. MANAGEMENT OF RENAL CALCULI Medical management • 85% of the time, it is possible to spontaneously pass a kidney stone with urination • Stones larger than 6 millimeters will almost always require some form of intervention, however. • Assuming there is no high-grade obstruction or associated infection in the urinary tract, and symptoms are relatively mild, various non-surgical measures can be used to encourage the passage of a stone.
  • 59. MANAGEMENT OF RENAL CALCULI… Analgesia  requires intravenous administration of NSAIDs or opioids in an emergency department setting.  Intravenous acetaminophen appears to be effective.
  • 60. MANAGEMENT OF RENAL CALCULI… Alpha adrenergic blockers  as tamsulosin (Flomax) may increase the spontaneous passage of the stone by 30%.
  • 61. MANAGEMENT OF RENAL CALCULI… Diuretics (dietary and medicinal)  One of the recognized medical therapies for prevention of stones is the thiazide diuretics.  Thiazides inhibit the formation of calcium-containing stones by reducing urinary calcium excretion, an effect independent of their diuretic properties.
  • 62. MANAGEMENT OF RENAL CALCULI… Urine alkalinization  The mainstay for medical management of uric acid stones is alkalinization (increasing the pH) of the urine. Uric acid stones are among the few types amenable to dissolution therapy, referred to as chemolysis.  Acetazolamide (Diamox) is a medication that alkalinizes the urine.
  • 63. MANAGEMENT OF RENAL CALCULI… Allopurinol  For people with hyperuricosuria and calcium stones, Allopurinol (Zyloprim) is one of the few treatments.
  • 64. MANAGEMENT OF RENAL CALCULI…  Allopurinol interferes with the production of uric acid in the liver.  The drug is also used in patients with gout or hyperuricemia (high serum uric acid levels).  Dosage is adjusted to maintain a reduced urinary excretion of uric acid.  Serum uric acid level at or below 6 milligrams/100 mL) is often a therapeutic goal for patients with gout or hyperuricemia.
  • 65. MANAGEMENT OF RENAL CALCULI…  Diet  for the calcium stones ( acid ash with limited intake of calcium and milk products  for oxalates stones ( alkaline ash with limited intake of foods high in oxalates  for uric acid stones ( alkaline ash with limited intake of foods high in purine  A high fluid of 3000ml per day after episode of urolithiasis to produce urine output of 2L per day  Intravenous therapy (fluid replacement )  Activity as tolerated
  • 66. MANAGEMENT OF RENAL CALCULI… Surgical management Invasive management Non invasive managements
  • 67. MANAGEMENT OF RENAL CALCULI… Surgical management Non invasive managements  Electro hydraulic lithotripsy  Ultrasonic lithotripsy  Laser impulse (holmium laser)  Extra corporeal shock wave lithotripsy
  • 68. MANAGEMENT OF RENAL CALCULI…  Electro hydraulic lithotripsy
  • 69. MANAGEMENT OF RENAL CALCULI…  Ultrasonic lithotripsy  Laser impulse  Extra corporeal shock wave lithotripsy Extracorporeal shock wave lithotripsy (ESWL) involves the use of a lithotriptor machine to deliver externally-applied, focused, high-intensity pulses of ultrasonic energy to cause fragmentation of a stone over a period of around 30–60 minutes.
  • 70. MANAGEMENT OF RENAL CALCULI… Surgical management Invasive managements  Percutaneous nephrostolithotomy  Cystolithophaxy  Pyelolithotomy (incision into renal pelvis)  Cystotomy(bladder calculi)  Nephrotomy  Ureteroscopic surgery
  • 71. MANAGEMENT OF RENAL CALCULI… Nursing management  Maintain proper nutrition  Force fluids 3 Liter / day  Assess renal status  Monitor and record vital signs, urine output, input and output, daily weight, specific gravity, lab studies, and urine pH.  Administer medication as prescribed  Allay the patient anxiety
  • 72. MANAGEMENT OF RENAL CALCULI…  Continue straining urine and giving warm baths and warm soaks to flanks to reduce pain Instruct on home care Increase fluid intake during hot Weather, illness, and exercise Void when urge is felt Test urine PH Increase fluid at night and void frequently
  • 73. NURSING DIAGNOSIS • Acute pain related to irritation of stone and inadequate pain control or comfort as manifested by complaints of pain, facial grimicing, restlessness. • Ineffective therapeutic regimen management related to lack of knowledge about prevention, recurrence, diet, fluid requirement as manifested by questions that indicate lack of knowledge.

Editor's Notes

  1. Occupation: prevents a person from maintaining adequate degree of hydration and when it leads to a large amount of extra renal fluid loss. Such occupations would include construction work, farming and other activities that keep people out in hot weather and increased sweating. Family history :cystinuria which is an inherited metabolic disorder. Small bowel disease i.e... Krohn’s disease associated steattorhea. The fatty acids in the gut bind with intraluminal calcium leaving the oxalate in a more easily absorbed state. hypercalcuria and hyperparathyroidism, that lead to increased calcium stone formation, gout, can produce uric acid stones.