Nephro

Renal Blood Flow

-       Renal blood flow normally drains ~20% of the cardiac output, or 1000 mL/min.

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Tuberoglomerular Feedback

-       Tubuloglomerular feedback (TGF) is mediated by specialized cells in the thick ascending limb of the loop of Henle called the macula densa that act as sensors of solute concentration and tubular fluid flow rate.

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Transport Systems

-       2 types of transport:

·      Movement of fluid and solutes sequentially across the apical and basolateral cell membranes (or vice versa) mediated by transporters, channels, or pumps is called cellular transport.

·      By contrast, movement of fluid and solutes through the narrow passageway between adjacent cells is called paracellular transport. Paracellular transport occurs through tight junctions, indicating that they are not completely “tight” or occlusive.

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Target transporters of condition/drug:

·      NaK2Cl co-transport of THICK ASCENDING LIMB – Bartter’s syndrome Type I, Loop Diuretics/Furosemide

·      Na-Cl co-transporter of DISTAL CONVOLUTED TUBULE – Gitelman syndrome, Thiazide

·      Epithelial Na Channel of COLLECTING DUCT – Liddle’s syndrome, Amiloride

·      Sodium bicarbonate cotransporter - Proximal renal tubular acidosis

·      Glucose transporter, GLUT2 - Fanconi-Bickel syndrome

·      Cystine, dibasic and neutral amino acid transporter – Cystinuria Type I

·      Neutral amino acid transporter – Hartnup Disorder

·      Renal Hypouricemia Type I - Urate-anion exchanger

·      Renal Hypouricemia Type II - Urate transporter, GLUT9

 ​

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Multiple Choice

Identify target TRANSPORTER?

Bartter’s syndrome Type I, Loop Diuretics/Furosemide

• NaK2Cl co-transport of THICK ASCENDING LIMB

• Na-Cl co-transporter of DISTAL CONVOLUTED TUBULE

• Epithelial Na Channel of COLLECTING DUCT

• Sodium bicarbonate cotransporter

Multiple Choice

Identify Target transporters of condition/drug

Fanconi-Bickel syndrome

• Glucose transporter, GLUT2

• Neutral amino acid transporter

• Urate-anion exchanger

•     Urate transporter, GLUT9

Multiple Choice

Identify Target transporters of condition/drug

Renal Hypouricemia Type II

• Glucose transporter, GLUT2

• Neutral amino acid transporter

• Urate-anion exchanger

•     Urate transporter, GLUT9

Multiple Choice

DRUG which causes PRE-RENAL AKI - CYCLOSPORINE

• Cyclophoshamide

• Cyclosporine

• Cisplatin

• Omeprazole

Multiple Choice

Feature consistent with PRE-RENAL AKI

• BUN/creatinine ratio below 20

• FeNa >1%,

• Hyaline Casts

• urine osmolality <500 mOsm/kg

PRE-RENAL AKI

BUN/creatinine ratio above 20, FeNa <1%, hyaline casts in urine sediment, urine specific gravity >1.018, urine osmolality >500 mOsm/kg ​

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Hepatorenal Syndrome

HEPATORENAL SYNDROME

TYPE 1 - A particularly poor prognosis is seen in the case of type 1 hepatorenal syndrome, in which AKI, defined as >two- fold increase in SCr to >2.5 mg/dL, within 2 weeks without an alternate cause (e.g., shock and nephrotoxic drugs), persists despite volume administration and withholding of diuretics.

TYPE 2 - a less severe form characterized mainly by refractory ascites

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Fill in the Blank

What TYPE of Hepatorenal Syndrome is >two- fold increase in SCr to >2.5 mg/dL, within 2 weeks without an alternate cause?

Multiple Choice

IDENTIFY USUAL STRUCTURE OF KIDNEY THAT IS DAMAGED in

Legionella infection, Severe pyelonephritis, Sepsis

• Small Vessels

• Tubules

• Intratubular

• Interstitium

Effect of SEPSIS and AKI:

The hemodynamic effects of sepsis—arising from generalized arterial vasodilation, mediated in part by cytokines that upregulate the expression of inducible NO synthase in the vasculature—can lead to a reduction in GFR.

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Fill in the Blank

Part of Kidney which is the MOST HYPOXIC?

ISCHEMIA and AKI:

The kidneys are also the site of one of the most hypoxic regions in the body, the renal medulla.

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CONTRAST-INDUCED NEPHROPATHY

The most common clinical course of contrast nephropathy is characterized by a RISE in SCr beginning 24–48 h following exposure, PEAK within 3–5 days, and resolving within 1 week.

 

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DRUGS AND AKI: AMINOGYCOSIDES

·      Aminoglycosides are freely filtered across the glomerulus and then accumulate within the renal cortex, where concentrations can greatly exceed those of the plasma.

·      AKI typically manifests after 5–7 days of therapy and can present even after the drug has been discontinued.

·      Hypomagnesemia is a common finding.

 

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DRUGS AND AKI: AMPHOTERICIN B

·      Causes renal vasoconstriction from an increase in tubuloglomerular feedback as well as direct tubular toxicity mediated by reactive oxygen species.

·      Drug binds to tubular membrane cholesterol and introduces pores.

· Clinical features of amphotericin B nephrotoxicity include polyuria, hypomagnesemia, hypocalcemia, and nongap metabolic acidosis. 

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DRUGS AND AKI: IFOSFAMIDE

·            May cause hemorrhagic cystitis and tubular toxicity, manifested as type II renal tubular acidosis (Fanconi’s syndrome), polyuria, hypokalemia, and a modest decline in GFR.

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DRUGS AND AKI: BEVACIZUMAB

·      Antiangiogenesis agents can cause proteinuria and hypertension via injury to the glomerular microvasculature (thrombotic microangiopathy).​

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Multiple Choice

Which of the ff. drug can cause FANCONI's SYNDROME?

• Aminoglycosides

• Amphotericin B

• Ifosfamide

• Bevacizumab

TOXIC AGENTS:

- Ethylene glycol, present in automobile anti-freeze, is metabolized to oxalic acid, glycolaldehyde, and glyoxylate, which may cause AKI through direct tubular injury and tubular obstruction. The metabolite 2-hydroxyethoxyacetic acid (HEAA) is thought to be responsible for tubular injury.

​

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TOXIC AGENTS:

​- Aristolochic acid was found to be the cause of “Chinese herb nephropathy” and “Balkan nephropathy” due to contamination of medicinal herbs or farming.

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DEFINITION OF AKI

By current definitions the presence of AKI is defined by an elevation in the SCr concentration or reduction in urine output. AKI is currently defined by a rise from baseline of at least 0.3 mg/dL within 48 h or at least 50% higher than baseline within 1 week, or a reduction in urine output to <0.5 mL/kg per h for longer than 6 h.

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Fill in the Blank

A patient presents with Livedo Reticularis, Retinal Plaque, Palpable Purpura with recent history of angioplasty. Diagnosis?

Fill in the Blank

A patient who presents with bloody diarrhea, schistocytes, elevated LDH, anemia and thrombocytopenia with elevated creatinine. Diagnosis of this condition involves screening for disease activity of?

Multiple Choice

IDENTIFY URINARY SEDIMENT

Malignant Infiltration of Kidney

• RBC cast

• WBC cast

• Granular Cast

• Eosinophil

Fill in the Blank

IDENTIFY URINARY SEDIMENT

Ethylene Glycol Intoxication

Fill in the Blank

NOVEL BIOMARKER detected in the plasma and urine within 2 h of cardiopulmonary bypass– associated AKI

NOVEL BIOMARKERS

•    Kidney injury molecule-1 (KIM-1) is a type 1 transmembrane protein that is abundantly expressed in proximal tubular cells injured by ischemia or nephrotoxins such as cisplatin.

​

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NOVEL BIOMARKERS

• Neutrophil gelatinase associated lipocalin (NGAL, also known as lipocalin-2 or siderocalin) is another novel biomarker of AKI. NGAL was first discovered as a protein in granules of human neutrophils. NGAL can bind to iron siderophore complexes and may have tissue-protective effects in the proximal tubule. NGAL is highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2 h of cardiopulmonary bypass– associated AKI.​

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Multiple Choice

Metabolic acidosis in AKI is generally not treated unless severe defined as

• pH <7.20 and serum bicarbonate <15 mmol/L

• pH <7.10 and serum bicarbonate <10 mmol/L

• pH <7.20 and serum bicarbonate <10 mmol/L

• pH <7.10 and serum bicarbonate <15 mmol/L

PROTEIN INTAKE AND AKI

• ·      Protein intake should vary depending on the severity of AKI:

  - 0.8–1.0 g/kg per day in noncatabolic AKI without the need for dialysis

  -  1.0–1.5 g/kg per day in patients on dialysis

  - up to a maximum of 1.7 g/kg per day if hypercatabolic and receiving continuous renal replacement therapy.

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Multiple Choice

Identify Protein Intake in patients on dialysis

• 0.8–1.0 g/kg per day

• 1.0–1.5 g/kg per day

• up to a maximum of 1.7 g/kg per day

• up to a maximum of 2.5 g/kg per day

BONE MANIFESTATIONS OF CKD

• ·      OSTEITIS FIBROSA CYSTICA

  - classic lesion of secondary hyperparathyroidism

  • ​Bone histology shows abnormal osteoid, bone and bone marrow fibrosis, and in advanced stages, the formation of bone cysts, sometimes with hemorrhagic elements so that they appear brown in color, hence the term brown tumor.

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BONE MANIFESTATIONS OF CKD

• ·      OSTEITIS FIBROSA CYSTICA

  • Clinical manifestations of severe hyperparathyroidism include bone pain and fragility, brown tumors, compression syndromes, and erythropoietin (EPO) resistance in part related to the bone marrow fibrosis. Furthermore, PTH itself is considered a uremic toxin, and high levels are associated with muscle weakness, fibrosis of cardiac muscle, and nonspecific constitutional symptoms.

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BONE MANIFESTATIONS OF CKD

• ·      OSTEITIS FIBROSA CYSTICA

  • TREATMENT: The optimal management of secondary hyperparathyroidism and osteitis fibrosa is prevention.

  • low-phosphate diet as well as the appropriate use of phosphate-binding agents.

  • Current National Kidney Foundation Kidney Disease Outcomes Quality Initiative guidelines recommend a target PTH level between 150 and 300 pg/mL (NOT to normal levels)

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BONE MANIFESTATIONS OF CKD

• ·      OSTEOMALACIA

  Reduced action of the active forms of vitamin D

• ​ADYNAMIC BONE DISEASE

  Low bone turnover with low or normal PTH levels

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Multiple Choice

Identify Bone Manifestation:

Due to reduced action of the active forms of vitamin D in CKD

• Osteitis Fibrosa Cystica

• Osteomalacia

• Adynamic Bone Disease

• Osteoporosis

RISK OF CV DISEASE with CKD

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​TRADITIONAL ( CLASSIC)	​NON-TRADITIONAL (CKD)
​hypertension	​anemia
​hypervolemia	​hyperphosphatemia
​sympathetic overactivity	​hyperparathyroidism
​dyslipidemia	​increased FGF-23
​hyperhomocysteinemia	​sleep apnea
​	​generalized inflammation

Multiple Choice

Which of the ff. is a TRADITIONAL risk factor for CV?

• generalized inflammation

• increased FGF-23

• hyperhomocysteinemia

• anemia

Fill in the Blank

a devastating condition seen almost exclusively in patients with advanced CKD. It is heralded by livedo reticularis and advances to patches of ischemic necrosis, especially on the legs, thighs, abdomen, and breasts

Anemia and CKD

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​- A normocytic, normochromic anemia is observed as early as stage 3 CKD and is almost universal by stage 4. The primary cause is insufficient production of EPO by the diseased kidneys.

Current practice is to target a Hgb of 100–115 g/L​

Neuromuscular Abnormalities and CKD

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• Subtle clinical manifestations of uremic neuromuscular disease usually become evident at stage 3 CKD

• Peripheral neuropathy usually becomes clinically evident after the patient reaches stage 4 CKD

  ​

Fill in the Blank

characterized by ill-defined sensations of sometimes debilitating discomfort in the legs and feet relieved by frequent leg movement seen in CKD pxs

Multiple Choice

At what level of CKD do you observe PERIPHERAL NEUROPATHY?

• Stage 2

• Stage 3

• Stage 4

• Stage 5

Multiple Choice

When the GFR has declined what GFR, pregnancy is associated with a high rate of spontaneous abortion?

• ~50 mL/min

• ~40 mL/min

• ~30 mL/min

• ~20 mL/min

Fill in the Blank

A skin condition unique to CKD patients consists of progressive subcutaneous induration, especially on the arms and legs.

CONTRAINDICATIONS for RENAL BIOPSY

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• In the patient with bilaterally small kidneys, renal biopsy is not advised because (1) it is technically difficult and has a greater likelihood of causing bleeding and other adverse consequences, (2) there is usually so much scarring that the underlying disease may not be apparent, and (3) the window of opportunity to render disease-specific therapy has passed.

  ​

CONTRAINDICATIONS for RENAL BIOPSY

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​

• Other contraindications to renal biopsy include uncontrolled hypertension, active urinary tract infection, bleeding diathesis (including ongoing anticoagulation), and severe obesity.

  ​

Multiple Choice

Contraindications for Renal Biopsy EXCEPT

• Uncontrolled Hypertension

• Uncontrolled Diabetes

• Active UTI

• Severe Obesity

Fill in the Blank

A fraction of the excess incidence of ESRD in African Americans is likely related to transmission of high-risk alleles for what gene

Multiple Choice

The most common acute complication of hemodialysis particularly among patients with diabetes mellitus

• Hypoglycemia

• Hypotension

• Chest Pain

• Cramps

DIALYZER reaction:

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​

• Type A reactions are attributed to an IgE- mediated intermediate hypersensitivity reaction to ethylene oxide used in the sterilization of new dialyzers

• Typically occurs soon after the initiation of a treatment (within the first few minutes) and can progress to full-blown anaphylaxis if the therapy is not promptly discontinued

  ​Treatment with steroids or epinephrine may be needed if symptoms are severe.

DIALYZER reaction:

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​

​

• Type B reaction consists of a symptom complex of nonspecific chest and back pain, which appears to result from complement activation and cytokine release.

• These symptoms typically occur several minutes into the dialysis run and typically resolve over time with continued dialysis.

PD Peritonitis:

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​

​Peritonitis is usually defined by an elevated peritoneal fluid leukocyte count (100/mm3, of which at least 50% are polymorphonuclear neutrophils)​

• these cutoffs are lower than in spontaneous bacterial peritonitis because of the presence of dextrose in peritoneal dialysis solutions and rapid bacterial proliferation in this environment without antibiotic therapy.

Multiple Choice

Identify Immunosuppressive Drug for KT

MACROLIDE Calcineurin Inhibitor with increased risk for Diabetes

• Cyclosporine

• Azathoprine

• Tacrolimus

• Belatacept

Multiple Choice

Identify Immunosuppressive Drug for KT

Causes Posttransplant Lymphoproliferative Disease (PTLD)

• Cyclosporine

• Azathoprine

• Tacrolimus

• Belatacept

Multiple Choice

Which of the ff. is an Opportunistic Infections in Renal Transplant Recipients occurring EARLY (1-6 months)?

• Cytomegalovirus

• Herpes zoster

• BK virus (polyoma)

• Urinary tract infection

STAIN

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STAIN	INDICATION
hematoxylin and eosin	cellularity and architecture
periodic acid–Schiff	stain carbohydrate moieties in the membranes of the glomerular tuft and tubules
Jones Methenamine Silver	​enhance basement membrane structure
Congo Red	Amyloid Deposits
Masson’s trichrome	Collagen Deposits

Multiple Choice

Which of the ff. STAIN enhances the BASEMENT membrane?

• Hematoxylin Eosin

• Congo REd

• Masson's Trichome

• Jones Methenamine Silver

Multiple Choice

Grossly, the kidneys have subcapsular hemorrhages with a “flea-bitten” appearance, and micros- copy on renal biopsy reveals focal proliferation around foci of necrosis associated with abundant mesangial, subendothelial, and subepithelial deposits DIAGNOSIS?

• Endocarditis-associated glomerulonephritis

• Post-streptococcal Glomerulonephritis

• IgA Nephropathy

• Good Pasture Syndrome

Multiple Choice

What CLASS of Lupus Nephritis?

Thickened basement membranes with diffuse subepithelial immune deposits; may occur with class III or IV lesions and is sometimes called mixed membranous and proliferative nephritis

• Class II

• Class III

• Class IV

• Class V

Multiple Choice

What CLASS of Lupus Nephritis?

commonly have high anti- DNA antibody titers, low serum complement, hematuria, red blood cell casts, proteinuria, hypertension, and decreased renal function; 50% of patients have nephrotic-range proteinuria. Patients with crescents on biopsy often have a rapidly progressive decline in renal function. Without treatment, this aggressive lesion has the worst renal prognosis.

• Class II

• Class III

• Class IV

• Class V

Multiple Choice

What CLASS of Lupus Nephritis?

predisposed to renal-vein thrombosis and other thrombotic complications.

• Class II

• Class III

• Class IV

• Class V

Treatment for LUPUS nephritis

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​

​

Current evidence suggests that inducing a remission with administration of high- dose steroids and either cyclophosphamide or mycophenolate mofetil for 2–6 months, followed by maintenance therapy with lower doses of steroids and mycophenolate mofetil or azathioprine, best balances the likelihood of successful remission with the side effects of therapy.​

Multiple Choice

The target epitopes for this autoimmune disease, GOODPASTURE'S SYNDROME lie in the quaternary structure of

• a3 NC1 domain of collagen IV

• a4 NC1 domain of collagen IV

• a5 NC1 domain of collagen IV

• a6 NC1 domain of collagen IV

Multiple Choice

BEST accounts for the pathogenesis of sporadic IgA nephropathy

• O glycosylation of the hinge region of primarily polymeric IgA1

• A glycosylation of the hinge region of primarily polymeric IgA1

• B glycosylation of the hinge region of primarily polymeric IgA1

• X glycosylation of the hinge region of primarily polymeric IgA1

Multiple Choice

TREATMENT for IgA Nephropathy (Mild)

• Steroids

• Tonsillectomy

• ACE Inhibitors

• Supportive Tx

Fill in the Blank

small-vessel vasculitis is associated with peripheral eosinophilia, cutaneous purpura, mononeuritis, asthma, and allergic rhinitis

Multiple Choice

Most common and proliferative of types of MPGN shows mesangial proliferation with lobular segmentation on renal biopsy and mesangial interposition between the capillary basement membrane and endothelial cells usually assoc with HEPATITIS C

• Type I

• Type II

• Type III

• Type IV

Multiple Choice

Also known as DENSE DEPOSIT DISEASE type of MPGN

• Type I

• Type II

• Type III

• Type IV

Multiple Choice

sometimes known as nil lesion

• Minimal Change Disease

• IgA Nephropathy

• PSGN

• MPGN

Multiple Choice

In 70% of cases, autoantibodies against the M-type phospholipase A2 receptor circulate and bind to a conformational epitope present in the PLA2R on human podocytes, producing characteristic in situ deposits.

• FSGS

• PSGN

• Membranous Nephropathy

• MPGN

Fill in the Blank

Some patients also develop eosinophilic, PAS+ nodules called nodular glomerulosclerosis or Kimmelstiel-Wilson nodule

Diagnosis?

Fill in the Blank

Definition of MICROALBUMINURIA

Fill in the Blank

an X-linked inborn error of globotriaosylceramide metabolism secondary to deficient lysosomal a-galactosidase A activity, resulting in excessive intracellular storage of globotriaosylcera- mide. Affected organs include the vascular endothelium, heart, brain, and kidneys. Presents in childhood in males with acroparesthesias, angiokeratoma, and hypohidrosis. These vacuoles of electron-dense materials in parallel arrays (ZEBRA BODIES) are easily seen on electron microscopy.

Fill in the Blank

Classically, patients develop hematuria, thin- ning and splitting of the GBMs, mild proteinuria (<1–2 g/24 h), which appears late in the course, followed by chronic glomerulosclerosis leading to renal failure in association with sensorineural deafness. Biopsy reveals multilamellations surrounding lucent areas that often contain granules of varying density—the so-called split basement membrane

Multiple Choice

The target epitopes for this autoimmune disease, ALPORT'S SYNDROME lie in the

• a5(IV) collagen chain

• a4(IV) collagen chain

• a3(IV) collagen chain

• a2(IV) collagen chain

Fill in the Blank

Syndrome that develop iliac horns on the pelvis and dysplasia of the dorsal limbs involving the patella, elbows, and nails, variably associated with neural-sensory hearing impairment, glaucoma, and abnormalities of the GBM and podocytes, leading tohematuria, proteinuria, and FSGS. The syndrome is autosomal dominant, with haploinsufficiency for the LIM

Multiple Choice

IDENTIFY associated Glomerular Lesion: INFLUENZA

• IgA Nephropathy

• Membranous Nephropathy

• MPGN

• Anti-GBM Disease

Multiple Choice

most commonly associated with clinical renal disease, and the glomerular lesions can be classified

• Schistosoma mansoni

• Schistosoma haematobium

• Schistosoma japonicum

• Schistosoma mekongi

ADPKD Criteria

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The presence of at least two renal cysts (unilateral or bilateral) is sufficient for diagnosis among at-risk subjects between 15 and 29 years of age with a sensitivity​value of 96% and specificity value of 100%. The presence of at least two cysts in each kidney and at least four cysts in each kidney, respectively, are required for the diagnosis among at-risk subjects aged 30–59 years and aged ≥60 years with a sensitivity value of 100% and specificity value

of 100%.

​

​

Multiple Choice

IDENTIFY CYSTIC disorder with Clinical features of:

Renal Cell Ca, Retinal angiomas; CNS hemangioblastomas; pheochromocytomas

• Tuberous Sclerosis

• Von Hippel-Lindau disease

• Bardet-Biedl syndrome

• Nephronophthisis

Multiple Choice

IDENTIFY CYSTIC disorder with Clinical features of:

Angiomyolipomas; renal cell carcinoma Facial angiofibromas; CNS hamartomas

• Tuberous Sclerosis

• Von Hippel-Lindau disease

• Bardet-Biedl syndrome

• Nephronophthisis

Multiple Choice

IDENTIFY CYSTIC disorder with Clinical features of:

CNS anomalies, polydactyly, congenital heart defects

• Meckel-Gruber syndrome

• Senior-Loken syndrome

• Bardet-Biedl syndrome

• Sensenbrenner syndrome

Multiple Choice

IDENTIFY CYSTIC disorder with Clinical features of:

Skeletal dysplasia; thoracic deformities; polydactyly; renal cysts; retinitis pigmentosa

• Meckel-Gruber syndrome

• Senior-Loken syndrome

• Bardet-Biedl syndrome

• Sensenbrenner syndrome

Multiple Choice

The ff. URINARY factors INCREASE risk fo NEPHROLITHIASIS EXCEPT

• High Urine Calcium

• High Urine Citrate

• High Urine Uric Acid

• High Urine Oxalate

Urine pH and stones

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Urine pH influences the solubility of some crystal types. Uric acid stones form only when the urine pH is consistently ≤5.5 or lower, whereas calcium phosphate stones are more likely to form when the urine pH is ≥6.5 or higher. Cystine is more soluble at higher urine pH. Calcium oxalate stones are not influenced by urine pH.

​

​

Multiple Choice

Urine pH influences the solubility of some crystal types.

Which of the ff. forms when the urine pH is consistently ≤5.5 or lower?

• Uric Acid

• Calcium Oxalate

• Calcium Phosphate

• Cystine

Multiple Choice

Urine pH influences the solubility of some crystal types.

Which of the ff. forms when the urine pH is not influenced by urine pH?

• Uric Acid

• Calcium Oxalate

• Calcium Phosphate

• Cystine

Multiple Choice

more common in patients with distal renal tubular acidosis and primary hyperparathyroidism.

• Uric Acid

• Calcium Oxalate

• Calcium Phosphate

• Cystine

Multiple Choice

RADIOLUSCENT

• Uric Acid

• Calcium Oxalate

• Calcium Phosphate

• Cystine

Multiple Choice

visible on plain radiographs and often manifest as staghorn calculi or multiple bilateral stones.

• Uric Acid

• Calcium Oxalate

• Calcium Phosphate

• Cystine

Fill in the Blank

preferred choice of Tx for CYSTINE stones due to its better adverse event profile

Multiple Choice

For large upper-tract stones, has the highest likelihood of rendering the patient stone-free.

• percutaneous nephrostolithotomy

• Extracorporeal shockwave lithotripsy (ESWL)

• Potassium Citrate

• Laser Fragmentation

Mimics

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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 con- fused with acute diverticulitis.

If the stone lodges in the ureter at the ureterovesical junction, the patient may experience urinary urgency and frequency. In female patients, the latter symptoms may lead to an incorrect diagnosis of bacterial cystitis; the urine will contain red and white blood cells, but the urine culture will be negative.

​

Multiple Choice

Patient presents with RUQ pain. Utz revealed Nephrolithiasis located where?

• blocks ureter as it crosses over the right pelvic brim

• Ureterovesical junction

• Distal Right Ureter

• right ureteral pelvic junction