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Pathological Case Report: Nephrolithiasis (Renal Calculi)


COVER PAGE

Title: Nephrolithiasis with Acute Obstructive Uropathy: A Pathological Case Report Date: July 13, 2026 Speciality: Nephrology / Urology / Pathology

1. PATIENT DEMOGRAPHICS

ParameterDetails
NameMr. R.K. (identity anonymized)
Age38 years
SexMale
OccupationOffice worker (sedentary)
NationalityIndian
Date of AdmissionJuly 13, 2026
Presenting HospitalGeneral Hospital, Urology Department
Background Note: Nephrolithiasis is more common in men than women by a 2:1 ratio, with a peak age at the third to fourth decade. Predisposing medical conditions include diabetes mellitus, hypertension, metabolic syndrome, distal renal tubular acidosis, gout, and autosomal dominant polycystic kidney disease (ADPKD). - Washington Manual of Medical Therapeutics, p. 495

2. CHIEF COMPLAINT

"Severe left-sided flank pain since this morning, radiating to the groin, associated with blood in my urine and repeated vomiting."
Duration: Acute onset, 8 hours prior to admission Character: Colicky, severe (patient rated 9/10 on pain scale), intermittent waves Radiation: Left costovertebral angle → left flank → left groin → left testicle Associated symptoms: Nausea and vomiting (x3 episodes), gross hematuria, urinary urgency, dysuria

3. HISTORY OF PRESENTING ILLNESS

Mr. R.K. was a 38-year-old male with a 2-year history of recurrent episodes of left flank pain. He presented with an acute, severe onset of left flank pain that woke him from sleep at 5:00 AM. The pain was colicky in nature, rated 9/10 in severity, and radiated from the left costovertebral angle (CVA) to the left groin and left scrotum. He noted dark, reddish urine when attempting to void, with associated urinary urgency and a burning sensation on urination. He had two prior similar episodes in the past 2 years, one of which resolved spontaneously with the passage of what he described as a "small gravel-like stone." He reported no fever, no chills, no dysuria beyond the current episode, and no prior urological procedures.
Dietary History: High dietary intake of animal protein, oxalate-rich foods (spinach, nuts), low daily water intake (~1 L/day), high sodium diet.
Family History: Father had kidney stones.
Past Medical History: Hypertension (on amlodipine), BMI 29.4 kg/m² (overweight), no diabetes mellitus.
Medications: Amlodipine 5 mg once daily.
Allergies: No known drug allergies.
Social History: Minimal physical activity; desk job; lives in a hot, humid climate (known to concentrate urine).

4. PHYSICAL EXAMINATION

4.1 General Appearance

  • Patient in significant distress, writhing in pain, unable to find a comfortable position (classic "restless" appearance of renal colic, distinguishing it from peritonitis where the patient lies still)
  • Pale, diaphoretic
  • Not jaundiced, not cyanosed

4.2 Vital Signs

ParameterValueReference
Temperature37.2°CNormal
Blood Pressure148/90 mmHgElevated (pain-related)
Heart Rate102 bpmTachycardia
Respiratory Rate18/minNormal
SpO₂98% on room airNormal
Pain Score9/10Severe

4.3 Systemic Examination

Abdomen:
  • Soft, non-rigid (no peritonism)
  • Left flank tenderness +++, especially over the left costovertebral angle
  • Murphy's punch test (renal punch sign) - Positive on the left - sharp pain elicited on percussion of the left CVA
  • No palpable abdominal mass
  • Bowel sounds present and normal
Renal / Urological:
  • No suprapubic tenderness
  • No palpable bladder distension
  • External genitalia: normal, no scrotal swelling or tenderness
Cardiovascular: S1 S2 regular, no murmurs; no peripheral edema Respiratory: Bilateral air entry equal, no adventitious sounds Neurological: Alert and oriented x3; no focal deficit

5. INVESTIGATIONS

5.1 Urinalysis

TestResultSignificance
ColorRed/smokyHematuria
ClarityTurbidCrystals/blood
pH5.5 (acidic)Favors calcium oxalate / uric acid stones
Specific Gravity1.032Concentrated urine
Blood (dipstick)3+Significant hematuria
ProteinTraceMild, non-nephrotic
Leucocytes2+Mild pyuria
NitritesNegativeNo active infection
GlucoseNegative-
Urine Microscopy:
  • RBCs: 50-100/HPF, non-dysmorphic (indicating non-glomerular source - stones vs. lower urinary tract)
  • WBCs: 10-15/HPF
  • Calcium oxalate crystals: Present - dumbbell-shaped / envelope-shaped crystals (paired pyramids viewed on end)
  • No RBC casts (excludes glomerulonephritis)
Urine Culture: Pending (no growth at 48 hours - excludes active infection)
Note: Approximately 95% of patients with acute renal colic have hematuria. - Grainger & Allison's Diagnostic Radiology, p. 719

5.2 Serum Biochemistry

TestResultReference Range
Serum Creatinine1.3 mg/dL0.7-1.2 mg/dL (mildly elevated)
BUN (Urea Nitrogen)22 mg/dL7-20 mg/dL
eGFR68 mL/min/1.73 m²Stage G2 mild reduction
Serum Calcium10.8 mg/dL8.5-10.5 mg/dL (mildly elevated)
Serum Phosphate3.1 mg/dL2.5-4.5 mg/dL (normal)
Serum Uric Acid7.4 mg/dL3.5-7.2 mg/dL (elevated)
Serum PTH (iPTH)52 pg/mL15-65 pg/mL (upper normal)
Serum Magnesium1.8 mg/dL1.7-2.2 mg/dL (normal)
Serum Sodium140 mEq/L136-145 (normal)
Serum Potassium4.1 mEq/L3.5-5.0 (normal)
Venous bicarbonate22 mEq/L22-26 (normal)
Serum Albumin4.1 g/dLNormal
CBCWBC 9,800/mm³Normal; no leucocytosis
Note: Mild hypercalcemia warrants further evaluation for primary hyperparathyroidism as a causative factor. PTH in the upper range in setting of high-normal calcium is "inappropriately normal" and suggests primary hyperparathyroidism may be contributing.

5.3 Imaging Studies

Plain Abdominal X-Ray (KUB - Kidneys, Ureters, Bladder):
  • A radio-opaque density noted at the left ureteropelvic junction (UPJ), approximately 6 mm in diameter
  • Mild soft tissue haziness in the left renal fossa
  • Limitation: Plain radiography has a sensitivity of only 60% for renal stones. - Grainger & Allison's Diagnostic Radiology, p. 719
Renal Ultrasound:
  • Left kidney: Mild hydronephrosis (Grade II), increased echogenicity at the renal pelvis
  • Left ureteral stone identified at UPJ with posterior acoustic shadowing (~6 mm)
  • Right kidney: Normal echogenicity, no hydronephrosis
  • Bladder: Normal wall, no intraluminal mass
  • Limitation: May miss stones <3 mm. Safe and readily available. - Washington Manual, p. 496
Non-Contrast CT Abdomen/Pelvis (Stone Protocol CT) - Gold Standard:
  • Left UPJ stone: 6 mm, hyperdense, 550 HU - consistent with calcium oxalate stone (most calcium-containing stones: 150-1000 HU)
  • Mild left hydroureter proximal to the stone
  • Grade II left hydronephrosis
  • Periureteral fat stranding (sign of edema and obstruction)
  • Right kidney and ureter: Normal
  • No secondary signs of perforation or rupture
  • Conclusion: Non-contrast CT is the one-stop imaging study of choice for renal and ureteric stone evaluation. - Grainger & Allison's Diagnostic Radiology, p. 719

5.4 24-Hour Urine Collection (Outpatient, 3 Weeks Later - Patient on Usual Diet)

ParameterResultTarget
Urine Volume1.2 L/24h>2.0 L/24h (low - major risk factor)
Urinary Calcium320 mg/24h<250 mg/24h (hypercalciuria)
Urinary Oxalate48 mg/24h<40 mg/24h (mild hyperoxaluria)
Urinary Citrate280 mg/24h>320 mg/24h (hypocitraturia)
Urinary Sodium210 mEq/24h<100 mEq/24h (high - drives calcium excretion)
Urinary Uric Acid750 mg/24h<750 mg/24h (borderline hyperuricosuria)
Urinary pH5.4-
This collection is reserved for when the patient is on their usual outpatient diet, not during an acute episode. - Washington Manual, p. 496

5.5 Stone Analysis (Stone Passed Spontaneously)

  • Composition: 85% Calcium Oxalate Monohydrate (whewellite), 15% Calcium Oxalate Dihydrate (weddellite)
  • Size: 5 x 4 mm
  • Shape: Rough, irregular, yellowish-brown
  • Consistency: Hard
  • Gross appearance: Irregular surface with spiky projections (characteristic of calcium oxalate monohydrate)
Pathological Findings on Passed Stone:
  • Calcium oxalate monohydrate - the most common form in most populations
  • Studies in India have shown >90% of calculi are calcium oxalate stones, predominantly calcium oxalate monohydrate (80%). - Brenner and Rector's The Kidney, p. 3769

6. DIAGNOSIS

Primary Diagnosis:

Nephrolithiasis - Left Ureteric Stone at UPJ (Calcium Oxalate Monohydrate, 6 mm) with Grade II Left Hydronephrosis

Contributing Metabolic Abnormalities:

  1. Idiopathic Hypercalciuria - urinary calcium 320 mg/24h
  2. Hypocitraturia - citrate 280 mg/24h (citrate is a natural inhibitor of calcium crystal growth)
  3. Mild Hyperoxaluria - oxalate 48 mg/24h
  4. Chronic Low Fluid Intake / Hypovolumic Concentrated Urine - volume 1.2 L/24h
  5. Possible borderline Primary Hyperparathyroidism - mildly elevated calcium + inappropriately normal PTH (further DEXA scan, sestamibi scan ordered as outpatient)

Differential Diagnoses Considered and Excluded:

DiagnosisReason Excluded
Ureteric transitional cell carcinomaCT showed only stone; no soft tissue mass; young patient
PyelonephritisNo fever, negative culture, no WBC casts
Renal papillary necrosisNo analgesic abuse history; no ring shadow on CT
Abdominal aortic aneurysmCT abdomen normal aorta; no pulsatile mass
AppendicitisRight side, normal appendix on CT
Ovarian/adnexal pathologyMale patient
Acute glomerulonephritisNon-dysmorphic RBCs, no casts, no proteinuria

7. PATHOLOGICAL MECHANISM AND STONE FORMATION

7.1 Types of Renal Stones and Their Pathology

Calcium-Based Stones (80% of all kidney stones):
  • Most common type: mixed calcium oxalate + calcium phosphate
  • Second: calcium oxalate alone
  • Third: calcium phosphate alone
  • Calcium oxalate crystals: Dumbbell-shaped or appear as paired pyramids (envelope appearance on end); found in acidic or alkaline urine; radio-opaque
  • Calcium phosphate crystals: Elongated, blunt crystals; form in alkaline urine
  • Washington Manual, p. 495
Uric Acid Stones (10%):
  • Develop in persistently acidic urine (pH <5.5)
  • Associated with metabolic syndrome, gout, myeloproliferative disorders
  • Radiolucent; crystal shapes - needles and rhomboid forms
  • Hypouricosuric states promote precipitation more by acidic pH than hyperuricemia
Struvite Stones (10%) - "Infection Stones":
  • Composed of magnesium ammonium phosphate ("triple phosphate")
  • Require urease-producing organisms: Proteus, Klebsiella, Serratia, Haemophilus, Pseudomonas
  • Form in alkaline urine (urea → NH₃ → alkalinizes urine)
  • Radio-opaque; can fill entire renal pelvis = staghorn calculus
  • Characteristic microscopy: coffin-lid shaped crystals
  • Associated with anatomic abnormalities (VUR, PUJ obstruction, ureteral stricture)
Cystine Stones (<1%):
  • Autosomal recessive disorder of renal tubular reabsorption
  • Defective reabsorption of dibasic amino acids: Cystine, Ornithine, Lysine, Arginine (mnemonic: COLA)
  • Only cystine is highly insoluble and precipitates in acidic urine
  • Intermediate radiolucency; hexagonal crystals on microscopy
  • Washington Manual, p. 496

7.2 Pathophysiology of Calcium Oxalate Stone Formation in This Patient

  1. Low urine volume → concentrated urine → supersaturation of calcium and oxalate
  2. Hypercalciuria (dietary/absorptive) → increased urinary calcium load
  3. Hypocitraturia → reduced chelation of urinary calcium → calcium available to bind oxalate
  4. Mild hyperoxaluria → dietary excess (spinach, nuts) → more substrate available
  5. Acidic urine → favors calcium oxalate monohydrate precipitation
  6. Net result: Crystal nucleation → crystal growth → aggregation → stone formation
  7. Stone migrates from renal pelvis → ureter → impaction at UPJ (narrowest point)
  8. Impaction → obstruction → ureteral smooth muscle spasm → renal colic
  9. Stone abrades urothelium → hematuria
  10. Persistent obstruction → hydronephrosis → risk of obstructive nephropathy

7.3 Nephrocalcinosis vs. Nephrolithiasis

FeatureNephrocalcinosisNephrolithiasis
LocationRenal parenchymaRenal collecting system
Medullary causesHyperparathyroidism, medullary sponge kidney, RTA, Vit D toxicity, primary hyperoxaluriaAs per stone type
Cortical causesAcute cortical necrosis, chronic GN, primary hyperoxaluria-
Prevalence95% medullary-
Grainger & Allison's Diagnostic Radiology, p. 719

8. MANAGEMENT

8.1 Acute Management (Emergency/Inpatient)

Step 1 - Analgesia:
  • IV Ketorolac 30 mg (NSAID - first-line for renal colic)
  • Oral/IV Morphine sulfate if NSAID contraindicated or pain uncontrolled
  • IV Ondansetron 4 mg for nausea and vomiting
Step 2 - Hydration:
  • IV Normal Saline 1 L over 2 hours (volume expansion to increase urine output)
  • Goal: Urine output >0.5 mL/kg/hour
Step 3 - Alpha-1 Blocker (Medical Expulsive Therapy - MET):
  • Tamsulosin 0.4 mg once daily (alpha-1 adrenergic blocker)
  • Relaxes ureteral smooth muscle → facilitates stone passage
  • Most effective for stones <10 mm in the distal ureter
Step 4 - Monitor:
  • Serial urine straining (to capture passed stone for analysis)
  • Repeat vital signs, pain assessment every 4-6 hours
  • Monitor urine output and creatinine
Indications for Urgent Urological Intervention:
  • Stone >10 mm (unlikely to pass spontaneously)
  • Concurrent urinary tract infection with obstruction (sepsis risk - urological emergency)
  • Bilateral obstruction or solitary kidney obstruction with AKI
  • Intractable pain / vomiting despite medical therapy
  • Washington Manual, p. 496

8.2 Surgical/Interventional Options

ProcedureIndicationDetails
Ureteroscopy + Laser Lithotripsy (URS)Ureteric stones, failed conservative therapyFlexible ureteroscope, holmium laser fragmentation
Extracorporeal Shock Wave Lithotripsy (ESWL)Renal/upper ureteric stones <2 cmExternal shockwaves fragment stone; non-invasive
Percutaneous Nephrolithotomy (PCNL)Large stones >2 cm, staghorn calculiPercutaneous access to renal pelvis
Ureteral Stenting (DJ Stent)Obstruction with infection/AKIBypasses stone; allows drainage
ESWL Complications to Monitor (post-procedure): Flank pain, nausea, vomiting (especially 48 hours after procedure), skin ecchymosis, gross hematuria (usually self-limited <24 hours), UTI, and rarely sepsis. - Tintinalli's Emergency Medicine, p. 194

8.3 Long-Term Prevention (Specific to This Patient - Calcium Oxalate Stone)

Foundation of therapy for ALL stone types:
  • Maintain high urine output: 2-3 L/day (the single most effective measure)
  • Low-sodium diet: 2-2.3 g/day (80-100 mmol/day) - excess sodium increases urinary calcium excretion
  • Washington Manual, p. 496
Specific measures for Calcium Oxalate Stones:
Metabolic ProblemIntervention
HypercalciuriaLow-sodium diet + Thiazide diuretic (hydrochlorothiazide 25 mg/day) - reduces renal calcium excretion
HypocitraturiaPotassium citrate 10-60 mEq/day in divided doses; OR lemon juice (4 oz in 1 L water daily)
Hyperoxaluria (dietary)Avoid oxalate-rich foods: spinach, rhubarb, nuts, chocolate, tea
Calcium intakeAge-appropriate dietary calcium intake (do NOT restrict dietary calcium - it binds oxalate in gut reducing absorption); avoid supplemental calcium tablets
Uric Acid Stone Prevention (if recurrence includes uric acid component):
  • Urinary alkalinization with potassium citrate to target urine pH 6.0-6.5
  • Low-protein diet
  • Xanthine oxidase inhibitors (allopurinol/febuxostat) if unresponsive to alkalinization
  • Washington Manual, p. 497
Dietary Counseling Summary for This Patient:
  • Increase water intake to >2.5 L/day
  • Reduce sodium to <2 g/day
  • Reduce animal protein
  • Maintain normal dietary calcium intake (1000 mg/day from food)
  • Avoid spinach, rhubarb, nuts, strong tea (oxalate sources)
  • Avoid vitamin C supplements >1 g/day (metabolized to oxalate)

8.4 Follow-Up Plan

TimelineAction
2 weeksRepeat renal ultrasound to confirm stone passage / resolution of hydronephrosis
3 weeks24-hour urine collection on usual diet (as performed above)
4 weeksEndocrinology referral for evaluation of primary hyperparathyroidism (DEXA scan, sestamibi parathyroid scan)
3 monthsRepeat serum calcium, PTH, creatinine
6 monthsReassess 24-hour urine while on treatment
OngoingAnnual review; urine pH monitoring at home; maintain hydration diary

9. DISEASE COMPLICATIONS (If Untreated)

ComplicationMechanism
HydronephrosisPersistent obstruction → back-pressure dilation
Obstructive Nephropathy / AKIPressure-related nephron damage
Chronic Kidney Disease (CKD)Repeated obstruction → irreversible tubular damage; nephrolithiasis responsible for 5% of all ESKD in northern India/Pakistan ("renal stone belt") - Brenner & Rector's, p. 3769
Pyelonephritis / UrosepsisStasis of infected urine proximal to obstructing stone
PyonephrosisInfected hydronephrosis - urgent drainage required
Renal Papillary NecrosisRecurrent obstruction + infection
HypertensionRenal parenchymal damage

10. SUMMARY TABLE

DomainKey Finding
Chief ComplaintSevere left flank pain radiating to groin + hematuria
Stone TypeCalcium oxalate monohydrate (85%)
Stone LocationLeft UPJ, 6 mm
Key InvestigationNon-contrast CT (gold standard), urine microscopy (envelope-shaped crystals), 24-hr urine
Metabolic DiagnosisHypercalciuria + hypocitraturia + mild hyperoxaluria
Acute TreatmentIV analgesia + hydration + tamsulosin (MET)
Definitive InterventionUreteroscopy + laser lithotripsy (if no spontaneous passage)
Long-Term PreventionHigh fluid intake, low-sodium diet, thiazide, potassium citrate
Complication RiskCKD, urosepsis, recurrence (50% at 5 years without prevention)

REFERENCES (Textbook Sources)

  • Washington Manual of Medical Therapeutics - Nephrolithiasis section, pp. 495-497
  • Grainger & Allison's Diagnostic Radiology - Renal Tract Calcifications, p. 719
  • Brenner and Rector's The Kidney, 2-Volume Set - Chronic Kidney Disease Due to Renal Calculi, p. 3769
  • Tintinalli's Emergency Medicine - Lithotripsy / Renal Colic section
  • Recent Systematic Review: Ungerer GN et al. "Mobile and eHealth technologies in the management and prevention of nephrolithiasis." Actas Urol Esp, 2024 [PMID: 37364768]
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