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Nephrolithiasis. Eva Jančová. Nephrolithiasis. Renal and ureteral stones are a common problem in primary care practice

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nephrolithiasis

Nephrolithiasis

Eva Jančová

nephrolithiasis1
Nephrolithiasis
  • Renal and ureteral stones are a common problem in primary care practice
  • Primary care physicians need to be alert to the possibility of nephrolithiasis and its consequences to decide upon a diagnostic approach, therapy, and refferal to a urologist or stone specialist
diagnosis and acute managment of suspected nephrolithiasis
Diagnosis and acute managment of suspected nephrolithiasis
  • Epidemiology
  • Etiology
  • Clinical manifestation
  • Differential diagnosis
  • Diagnosis
  • Acute therapy
  • Evaluation and subsequent treatment
diagnosis and acute managment of suspected nephrolithiasis1
Diagnosis and acute managment of suspected nephrolithiasis
  • Epidemiology
  • Etiology
  • Clinical manifestation
  • Differential diagnosis
  • Diagnosis
  • Acute therapy
  • Evaluation and subsequent treatment
epidemiology
Epidemiology
  • The prevalence of renal calculi varies with the population studied
  • The rate of nephrolihiasis increases with
    • age (is higher in men compared to woman)
    • whites compared to blacks
  • Patients discharged from hospital with diagnosis of stones
    • 1.8 per 10 000
  • Incidence of stones in general practice
    • 7 per 10 000
  • General practice incidence of stones in males aged 45–60 years
    • 21 per 10 000
diagnosis and acute managment of suspected nephrolithiasis2
Diagnosis and acute managment of suspected nephrolithiasis
  • Epidemiology
  • Etiology
  • Clinical manifestation
  • Differential diagnosis
  • Diagnosis
  • Acute therapy
  • Evaluation and subsequent treatment
etiology
Etiology
  • 85% of pts with n. form calcium stones
    • most of which are composed primary of calcium oxalate
    • less often calcium phosphate
  • The other main types include
    • Uric acid
    • Struvite (magnesium ammonium phosphate)
    • Cystine stone
  • The same pts may have more than one type of stone currently
    • Calcium and uric acid
major risk factors for calcium stones
Major Risk Factors for Calcium Stones
  • Low urine volume
  • Hypercalciuria
  • Hypocitraturia
  • Hyperuricosuria
  • Dietary factors
    • Low fluid intake
    • Type of fluid intake-soft drinks, apple or grapefruite juice
    • High protein intake
    • Low calcium intake
  • History of prior calcium stones
  • Hyperoxaluria (eg, enteric hyperoxaluria)
  • Meddulary sponge disease
  • Unexplained association with disorders-hypertension, vasectomy
other factors affect the risk of stone formation
Other factors affect the risk of stone formation
  • History of prior calcium nephrolithiasis
  • Family history of nephrolithiasis
  • Inhanced of entetric oxalate absorption
  • Urinary tract infection
  • Medivations /indinavir, sulfadiazine,…)
diagnosis and acute managment of suspected nephrolithiasis3
Diagnosis and acute managment of suspected nephrolithiasis
  • Epidemiology
  • Etiology
  • Clinical manifestation
  • Differential diagnosis
  • Diagnosis
  • Acute therapy
  • Evaluation and subsequent treatment
clinical presentations of urinary stones
Pain

Ureteric colic

Lumbar ache

On micturition

Haematuria

Sterile pyuria

Asymptomatic proteinuria

Dysuria and increased urinary frequency

Urinary tract infections

Acute (single or recurrent attack)

Chronic

Pyonephrosis

Calculus anuria

Strangury and interruption of urine stream

Clinical presentations of urinary stones
clinical manifestions
Patients may occasionally be diagnosed with asymtomatic nephrolithiasis

The asymptomatic phase is more likely persist in those who have never had a clinical episode of renal colic

Clinical manifestions
clinical manifestions symptoms
Patients occasionally present after already having passed gravel or a stone

Uric acid stones are more likely present with gravel but they cal also produce acute obstruction

Clinical manifestions-Symptoms
clinical manifestions1
Symptoms are usually produced when stones pass from the renal pelvis into the ureter

Pain is the most common symtom and varies from

a mild and barely noticeable ache,

to discomfort which is so intense that it requires hospitalization and parenteral medications

Clinical manifestions
clinical manifestions pain
The pain typically waxes and wanes in severity, and develops in waves or paroxysms that are related to movement of the stone in the ureter and associated ureteral spasm

Pain is thought to occur due to muscular contraction of the ureter in response to the stone

Clinical manifestions-Pain
clinical manifestions pain1
The site of obstruction determines the locaton of pain

Upper ureteral or renal pelvic obstruction lead to flak pain or tenderness

Lower ureteral obstruction causes pain that may radiate to the ipsilateral testicle or labia

The location of the pain may change as the stone migrates

Clinical manifestions-Pain
clinical manifestions pain2
Variable location of pain can be misleading and occasionally mimics an acute abdomen or dissectingClinical manifestions-Pain
clinical manifestions hematuria
Gross or microscopic hematuria occur in the majority of patients presenting with symptomatic nephrolithiasis

Unilateral flank pain, hematuria, and a positivity plain of the abdomen are present in 90 percent of emergency room patients with a stone

Absence of hematuria in the setting of acute flank pain does not exclude the presence of nephrolithiasis

Clinical manifestions-Hematuria
clinical manifestions2
Other symptoms

Nausea

Vommiting

Dysuria

Urgency

Complicantions

Persistent renal obstruction

Sepsis

Clinical manifestions
diagnosis and acute managment of suspected nephrolithiasis4
Diagnosis and acute managment of suspected nephrolithiasis
  • Epidemiology
  • Etiology
  • Clinical manifestation
  • Differential diagnosis
  • Diagnosis
  • Acute therapy
  • Evaluation and subsequent treatment
differential diagnosis
Differential diagnosis
  • Ectopic pregnancy
  • Aortic aneurysm
  • Acute intestinal obstruction
  • Renal carcinoma (bleeding within the kidney)
diagnosis and acute managment of suspected nephrolithiasis5
Diagnosis and acute managment of suspected nephrolithiasis
  • Epidemiology
  • Etiology
  • Clinical manifestation
  • Differential diagnosis
  • Diagnosis
  • Acute therapy
  • Evaluation and subsequent treatment
diagnosis
Diagnosis
  • The diagnosis of nephrolithiasis is initially suspected by clinical presentation
  • Confirmatory radiologic tests include
    • Abdominal plain film (KUB)
    • Intravenous pyelography (IVP)
    • Ultrasonography
    • CT scan (including spiral CT)
    • MRI
abdominal plain film kub
Abdominal plain film (KUB)

Will identify radiopaque stones

  • Calcium-containing stones
  • Struvite stones
  • Cystine stones
abdominal plain film kub1
Advantages

Readily available

Inxpensive

Limited radiation

Useful in acute setting

Disadvantages

Requies skilled radiologist to interpret

Limited sensitivity and specificity

Abdominal plain film (KUB)
intravenous pyelography ivp
Intravenous pyelography (IVP)
  • High sensitivity and specificity for detection of stones and provides data about the degree of obstruction
intravenous pyelography ivp1
Advantages

Useful in planning therapy and confirming diagnosis

Long established history as gold standard

Disadvantages

Moderately expensive

Intravenous contrast required

Moderate x-ray exposure

Intravenous pyelography (IVP)
ultrasonography
Advantages

Readily available

Roughly equivalent to IVP as a diagnostic test

Improved sensitivity with use of color Doppler

No radiation exposure

Good for hydronephrosis

Disadvantages

Moderately expensive

Poor performance with small stones

Requires skilled technician and radiologist

Ultrasonography
ct scan including spiral ct
Advantages

Probably new gold standard

Can distinguish radiolucent stones from blood and tumor

Disadvantages

Expensive

Moderate x-ray exposure

Not uniform available

CT scan (including spiral CT)
slide30
Advantages

Great potential for localizing sight of stone in ureter

Disadvantages

Vera expensive

Largely investigational so far except in certain centres

MRI
results of diagnostic imaging in patients presenting with renal colic
Results of diagnostic imaging in patients presenting with renal colic

Sites of calcific lesions which may be confused with radio-opaque urinary stones:

  • gallstones, costal cartilages, mesenteric lymph nodes, adrenals, pancreas, renal and splenic arteries, pelvic veins.

The radiotranslucent stones

  • uric acid, xanthine, oxipurinol, 2,8-dihydroxyadenine, orotic acid, and triamterine.

Finely stippled nephrocalcinosis suggests

  • long-standing hypercalcaemia

Dense coarse nephrocalcinosis suggests

  • primary hyperoxaluria or renal tubular acidosis.
results of diagnostic imaging in patients presenting with renal colic1
Results of diagnostic imaging in patients presenting with renal colic

Obstructive uropathy due to:

  • Radio-opaque stone
  • Radiotranslucent obstructive lesion (stones, crystals, sloughed papillae, clots, carcinoma)
  • Generalized nephrocalcinosis
  • Medullary sponge kidney
  • Renal papillary necrosis (sloughed papilla)
  • Cortical scars due to chronic pyelonephritis
  • Renal carcinoma (cause of ‘clot colic’)
  • Coincidental calcific lesion (e.g. tuberculosis, Randall’s plaques)
diagnosis and acute managment of suspected nephrolithiasis6
Diagnosis and acute managment of suspected nephrolithiasis
  • Epidemiology
  • Etiology
  • Clinical manifestation
  • Differential diagnosis
  • Diagnosis
  • Acute therapy
  • Evaluation and subsequent treatment
acute therapy
Acute Therapy
  • Pain control
    • Nonsteroidal antiinflammatory drugs (NSAIDs)
    • Narcotics
  • Hydration
  • Urology consultation
acute therapy1
Acute Therapy
  • Patients can be managed at home if they are able to take oral medications and fluids
  • Hospitalization is required for those who
    • cannot tolerate oral intake
    • have very severe pain
acute therapy2
Acute Therapy
  • Hospitalization is required for those who
    • cannot tolerate oral intake
    • have very severe pain
urology consultation
Urology consultation

Urgent urologic consultation is warranted in patients with

  • Urosepsis
  • Acute renal failure

Outpatient urology referral is indicated in patients

  • Who fail to pass the stone after a trial of conservative management (usually two to four weeks)
  • A stone more 5mm in diameter
  • Uncontrolled pain
diagnosis and acute managment of suspected nephrolithiasis7
Diagnosis and acute managment of suspected nephrolithiasis
  • Epidemiology
  • Etiology
  • Clinical manifestation
  • Differential diagnosis
  • Diagnosis
  • Acute therapy
  • Evaluation and subsequent treatment
evaluation and subsequent treatment
Evaluation and subsequent treatment
  • The patient shoud be evaluated for possible underlying causes of stone disease
  • These include:
    • Hypercalcemia
    • Hypercalciuria
    • Hyperuricosuria
    • Hypocitraturia
    • Hyperoxaluria
evaluation and subsequent treatment calcium stones
Evaluation and subsequent treatment-Calcium stones
  • Composed purely or predominantly of calcium oxalate can occur in many differënt disordes
  • Calcium phosphate stones are associated with the same risk factors as calcum oxalate stones. One exception- calcium phosphate stones are more typical of complete or incomplete distal renal acidosis
calcium stones
Calcium stones
  • Oxalate crystals
urinary risk factors for idiopathic calcium stones
Urinary risk factors for idiopathic calcium stones
  • Low volume, which increased the concentrations of the lithogenic factors
  • Hypercalciuria, with or without hypercalcemia
  • Hyperuricosuria, which in calcium oxalate-stone formers, is usually due to increased protein intake and therefore uric acid production
  • Hypocitraturia, which can be marked in patients wih chronic metabolic acidosis
  • Hyperoxaluria, which may be present in up to 40 percent of male and 15 percent of female stone formers
  • Defects of macromolecular inhibitors
urinary risk factors for idiopathic calcium stones1
Urinary risk factors for idiopathic calcium stones
  • Calcium stone formation is most often idiopathic, but can occur a number of other disorders.
underlying systemic or renal disorders in calcium stone disease
Underlying systemic or renal disorders in calcium stone disease
  • Primary hyperparathyroidism
  • Medullary sponge kidney
  • Distal renal tubular acidosis (complete or incomplete)
  • Sarcoidosis (and other granulomatous diseases)
  • Hyperoxaluria
    • Enteric
    • Primary
evaluation and subsequent treatment u ric acid stones
Evaluation and subsequent treatment-Uric acid stones
  • Pure uric acid stones primary occur in patients in whom a persistently acid urine promotes uric acid precipitation
  • In the absence of gout, uric acid stones may be seen other causes of chronic overproduction of uric acid or in chronic diarrheal states in which bicarbonate loss and volume depletion lead to a concentrated, acid urine
caused of secondary due to increased purine biosynthesis and or urate production
Caused of Secondary due to increased Purine Biosynthesis and/or Urate Production
  • Inherited enzyme defects leading to purine overproduction
  • Clinical disorders leading to purine and/or overproduction
    • Myeloproliferative disorders
    • Lymfoproliferative disorders
    • Malignancies
    • Hemolytic disorders
    • Psoriasis
    • Obesity
    • Tissue hypoxia
    • Down Syndrome
    • Glycogen storage diseases (type III,V,VII)
caused of secondary due to increased purine biosynthesis and or urate production continue
Caused of Secondary due to increased Purine Biosynthesis and/or Urate Production-continue
  • Drug-,diet, or toxin-induced purine and /or urate overproduction
    • Ethanol
    • Excessive dietary purine ingestion
    • Pancreatic extract
    • Fructose
    • Vitamin B12 (pts with pernicious anemia)
    • Nicotinic acid
    • Cytotoxic drugs
    • Warfarin
evaluation and subsequent treatment s truvite stones
Evaluation and subsequent treatment-Struvite stones
  • Struvite stones only form in pts with a chronic urinary tract infection due to a urease production organism such as Proteus or Klebsiella
  • The stone may grow rapidly over a period of week to months and, if not, adequately treated, can develop into a staghorn or branched calculus involving the entire renal pelvis and calyces
evaluation and subsequent treatment cystine stones
Evaluation and subsequent treatment-Cystine stones
  • Cystine stones developt in pts with cystinuria due to the insolubility of cystine in the urine
  • The diagnosis of cystinuria is made from the family history, by identification of the pathognomonic hexagonal cystine crystal on urinalysis
cystine stones
Cystine stones
  • Typical hexagonal crystals of cystine under (a) non-polarized and (b) polarized light.
focused history
Focused History

All pts with a first stone should undergo a focused history to identify stone risk factors such as a family history of stone disease and certain dietary habits

  • Low fluid intake (high concetration of lithogenic factors)
  • High animal protein diet (which can lead to hypercalciuria, hyperuricosuria, hypocitraturia
  • High salt diet (which increases urinary calcium excretion)
  • Increased intake of oxalate-containing foods
  • Vitamin D supplements
investigations in a calcium stone former
Investigations in a Calcium Stone-former

Blood tests

  • Serum calcium 2-3x
  • Serum uric acid
  • Serum bicarbonate
  • Serum creatinine (electrolytes)
  • PTH
investigations in a calcium stone former1
Investigations in a Calcium Stone-former

Urinalysis

  • Urine microscopy and culture
  • Urine pH

24-hour collections (2-3x)

  • Volume
  • pH
  • creatinine
  • calcium
  • oxalate
  • uric acid
  • citrate
  • (sodium)
  • (urea)
methods for stone analysis
Methods for stone analysis
  • Wet chemical analysis (qualitative or quantitative)
  • Optical crystallography
  • X-ray diffraction
  • Thermogravimetric analysis
  • Scanning electron microscopy
  • IR spectroscopy
evaluation and subsequent treatment1
Evaluation and subsequent treatment
  • Subsequent therapy is based upon the type of stone and the biochemical abnormalities that are present
  • Therapy to prevent new stone formation is required:
    • All pts shoud increase fluid intake to above 2L/day, including drinking at night
    • Pts with calcium stones can be treated with a thiazide diuretic and low sodium diet for hypercalciuria, allopurinol for hyperuricosuria, and potassium citrate for hypocitraturia
evaluation and subsequent treatment2
Evaluation and subsequent treatment
  • Therapy to prevent new stone formation is required-continued:
    • Pts wit uric acid stones can bez treated with potassium citrate to alkalinize the urine ao allopurinol
    • Pts with cystine stones can be treated with high fluid intakem urinary alkalinizatin, and drugs such as penicillamine or captopril
    • Treatment of struvite stones is difficult
causes of macroscopic nephrocalcinosis cortical x medullary
Causes of macroscopic nephrocalcinosis (cortical x medullary)

Cortical

  • Chronic glomerulonephritis
  • Acute cortical necrosis
  • Chronic pyelonephritis
  • Benign nodular subcapsular
nephrocalcinosis
Nephrocalcinosis
  • Cortical nephrocalcinosis (necropsy specimen)
causes of macroscopic nephrocalcinosis cortical x medullary1
Medullary

Autonomous hyperparathyroidis

Milk alkali syndrome

Hypervitaminosis D

Sarcoidosis

Idiopathic hypercalciuria

MacGibbon–Lubinsky syndrome

Oxalosis

Distal renal tubular acidosis

Acetazolamide

Dent's disease

Hypomagnesaemia-hypercalciuria syndrome

Medullary sponge kidney

Renal papillary necrosis

Others (Williams' and Bartter's

Causes of macroscopic nephrocalcinosis (cortical x medullary)
nephrocalcinosis1
Nephrocalcinosis
  • Medullary nephrocalcinosis in a 25-year-old man with familial distal renal tubular acidosis.
prognosis for overall renal function continue
Prognosis for overall renal function-continue

Best

  • Idiopathic hypercalciuria
  • Medullary sponge kidney
  • Distal renal tubular acidosis
  • Autonomous hyperparathyroidism and other

rectifiable hypercalcaemias

  • Papillary necrosis
  • Dent’s disease/X-linked recessive nephrolithiasis
  • Hypomagnesaemia–hypercalciuria (Michelis–Manz)

syndrome

Worst

  • Primary hyperoxaluria, type 1
renal cell carcinoma
Renal Cell Carcinoma
  • Primary renal neoplasms
    • Renal cell carcinoma (80-85%)
    • Transitionla cell carcinoma (6%)
    • Oncocytomas
    • Collecting duct tumors
    • Rema sarcomas
    • Nephroblastomas
  • Secundary renal neoplasms
    • Rarelly
clinical features
Clinical features
  • Hematuria
  • Abdominal or flan mann
  • Scrotale varicocele
  • Vena cava involvement (ascies, hepatic dysfunction, pulmonary emboli)
  • Systemic or paraneoplastic syndroms
    • Fever
    • Cachexia
    • Amyloidosis
    • Anemie
    • Hepatic dysfunction
    • Erythrocytosis and thromocytosis
    • Hypercalcemia
    • Polymyalgia-like syndrome