Renal and urinary tract disorders

Answer 1

What is Acute Kidney Injury?

Abrupt loss of kidney function, defined as a rise in serum creatinine (SCr) of ≥0.3 mg/dL within 48 hours; a 50% increase in SCr within 7 days or urine output of <0.5 mL/kg/hr for >6 hours, resulting in retention of nitrogenous waste as well as electrolyte, acid–base, and volume homeostasis abnormalities

What conditions cause AKI

• poor kidney profusion
• damage to kidneys
• urine blockage in the kidney

What are the three categories of AKI with short descriptions and causes:

Prerenal (reduced renal perfusion, typically reversible) causes: Hypotension, volume depletion (GI losses, excessive sweating, diuretics, hemorrhage); renal artery stenosis/embolism; burns; heart/liver failure Decreased renal perfusion (often due to hypovolemia) leads to a decrease in glomerular filtration rate (GFR), which (if prolonged or severe) can progress to ischemic acute tubular necrosis (ATN).

Intrarenal (intrinsic kidney injury, often from prolonged or severe renal hypoperfusion) ATN (from prolonged prerenal azotemia, radiographic contrast material, aminoglycosides, NSAIDs, or other nephrotoxic substances), glomerulonephritis (GN), acute interstitial nephritis (AIN; drug induced), arteriolar insults, vasculitis, accelerated hypertension, cholesterol embolization (following an intra-arterial procedure), intrarenal deposition/sludging (uric acid nephropathy and multiple myeloma [Bence Jones proteins])

Postrenal (obstruction of the collecting system) Extrinsic compression (e.g., benign prostatic hypertrophy [BPH], carcinoma, pregnancy); intrinsic obstruction (e.g., calculus, tumor, clot, stricture, sloughed papillae); decreased function (e.g., neurogenic bladder), leading to obstruction of the urinary collection system

Risk Factors

• Chronic kidney disease (CKD)
• Comorbid conditions (e.g., diabetes mellitus 2, hypertension, heart failure, liver failure)
• Advanced age
• Radiocontrast material exposure (intravascular)
• Medications that impair autoregulation of GFR (NSAIDs, ACEI/ARB, cyclosporine/tacrolimus)
• Nephrotoxic medications (e.g., aminoglycoside antibiotics, platinum-based chemotherapy)
• Hypovolemia (e.g., diuretics, hemorrhage, GI losses)
• Sepsis, surgery, rhabdomyolysis
• Solitary kidney (risk in nephrolithiasis)
• BPH; malignancy (e.g., multiple myeloma)

What are some Commonly Associated Conditions?

Hyperkalemia, hyperphosphatemia, hypercalcemia, hyperuricemia, hydronephrosis, BPH, nephrolithiasis, congestive heart failure (CHF), uremic pericarditis, cirrhosis, CKD, malignant hypertension, vasculitis, drug reactions, sepsis, severe trauma, burns, transfusion reactions, recent chemotherapy, rhabdomyolysis, internal bleeding, dehydration

What might be found in the hx?

changes in PO intake, changes in urine output, and body weight.

verify any medication changes/hx

What may be evidence of Prerenal:

thirst, orthostatic symptoms

What may be evidence of Intrarenal:

nephrotoxic medications, radiocontrast material, other toxins

Livedo reticularis, SC nodules, and ischemic digits despite good pulses suggest atheroembolization.

Flank pain may suggest renal artery or vein occlusion.

What may indicate Postrenal?:

Colicky flank pain that radiates to the groin suggests ureteric obstruction such as a stone;

nocturia, frequency, and hesitancy suggest prostatic disease;

suprapubic and flank pain are usually secondary to distension of the bladder and collecting system;

anticholinergic drugs inhibit bladder emptying.

What are some uremic (increased levels of nitrogenous waste) symptoms?

lethargy, nausea/vomiting, anorexia, pruritus, restless legs, sleep disturbance, hiccups

What may Physical Exam show for uremic signs?

Uremic signs: altered sensorium, seizures, asterixis (tremor of an extended hand), myoclonus, pericardial friction rub, peripheral neuropathies

Prerenal?

Prerenal signs: tachycardia, decreased jugular venous pressure (JVP), orthostatic hypotension, dry mucous membranes, decreased skin turgor; comorbid stigmata of sepsis, liver disease, or heart failure

Intrinsic renal signs: pruritic rash, livedo reticularis, SC nodules, ischemic digits despite good pulses

Postrenal signs: suprapubic distension, flank pain, enlarged prostate

Diagnostic Tests & Interpretation

What are Initial Tests (lab, imaging)

CBC, BUN, SCr, electrolytes (including Ca/Mg/P); consider arterial or venous blood gas (ABG/VBG).

Compare to baseline renal function (creatinine [Cr]/GFR)

Urinalysis: dipstick for blood and protein; microscopy for cells, casts, and crystals

What are labs for Acute interstitial nephritis?

Sterile pyuria (especially WBC casts) suggests acute interstitial nephritis (AIN); triad of fever, rash, and eosinophilia present in 10% of cases. Casts: transparent hyaline casts—prerenal etiology; pigmented granular/muddy brown casts—ATN; WBC casts—AIN

What are labs for Glomerular nephritis or vasculitis?

Proteinuria, hematuria, and edema, often with nephritic urine sediment (RBCs and RBC casts), suggest GN or vasculitis. RBC casts—GN

What are Common lab abnormalities in AKI

Increased: K+, phosphate, Mg, uric acid

Decreased: Hgb, Na, Ca

What would you learn from a Renal ultrasound (US): first line; excludes postrenal causes; identifies kidney size, hydronephrosis (dialation of renal pelvis and calyces from obstruction), and nephrolithiasis

What would you learn from a Doppler-flow renal US; problems?: evaluates for renal artery stenosis/thrombosis; operator dependent

What would you learn from an Abdominal x-ray (kidney, ureter, bladder [KUB]): identifies calcification, renal calculi, kidney size

What is the Treatment

• Identify and correct prerenal and postrenal causes.
• Stop nephrotoxic drugs and renally dose others.
• Strictly monitor intake/output and daily weight.
• Optimize cardiac output to maintain renal perfusion.
• Optimize nutrition and treat any infections.

What are Indications for renal replacement therapy (RRT):

volume overload, severe or progressive hyperkalemia, or severe metabolic acidosis refractory to medical management; advanced uremic complications (pericarditis, encephalopathy, bleeding diathesis)

What is the first line Medication?

complicated . . . mostly inpatient or specialist

Second Line

Tamsulosin or other selective α-blockers for bladder outlet obstruction secondary to BPH

Answer 2

Chronic Kidney Disease

Basics

Chronic kidney disease (CKD) is defined as structural or functional abnormalities of the kidney for ≥3 months, as determined by either pathologic abnormalities or markers of damage—including abnormalities in blood or urine tests, histology, imaging studies, or history of kidney transplant—or a GFR <60 mL/min/1.73 m2 for ≥3 months.

What are the common electroyte and lab disorders?

• increased serum creatinine (surrogate maker of kidney function)
• increased BUN (with nor SCr, possible dehydration)
• hypernatrimia, hypercalcemia, hyperkalemia

Description

In 2012, Kidney Disease: Improving Global Outcomes (KDIGO) classified CKD in six categories by GFR estimation (in mL/min/1.73 m2):

G1: kidney damage with normal or increased GFR ≥90

G2: mild ↓ GFR 60 to 89

G3a: mild to moderate ↓ GFR 45 to 59

G3b: moderate to severe ↓ GFR 30 to 44

G4: severe ↓ GFR 15 to 29

G5: kidney failure: GFR <15 or dialysis

CKD per albumin-to-creatinine ratio (ACR) category:

A1: normal to mildly increased: <30 mg/g or <3 mg/mmol

A2: moderately increased: 30 to 300 mg/g or 3 to 30 mg/mmol

A3: severely increased: >300 mg/g or >30 mg/mmol

Risk of progression depends on comorbid conditions.

System(s) affected: renal/urinary, cardiovascular, skeletal, endocrine, metabolic, hematologic, lymphatic, immune, neurologic

Synonym(s): chronic renal failure; chronic renal insufficiency

Geriatric Considerations
GFR normally decreases with age, despite normal creatinine (Cr). Adjust renally cleared drugs for GFR in the elderly.

Pediatric Considerations
CKD definition is not applicable for children <2 years because of lower GFR even when corrected for body surface area. Calculated GFR based on serum Cr is used in this age group.

Pregnancy Considerations
Renal function in CKD may deteriorate during pregnancy. Cr >1.5 and hypertension (HTN) are major risk factors for worsening renal function.

Increased risk of premature labor, preeclampsia

ACE inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs) are contraindicated due to teratogenicity. Use diuretics with caution.

Epidemiology

African Americans are 3.6 times more likely to develop CKD than Caucasians.

Predominant sex: similar in both sexes; however, incidence rate of end-stage renal disease (ESRD) is 1.6 times higher in males than females.

Incidence
Estimated annual incidence of 1,700/1 million population

Prevalence
Overall prevalence of CKD is 14.2%. Unadjusted prevalence/incidence rates of ESRD (stage 5) are 1,752 and 362.4/1 million, respectively. Numbers do not reflect the burden of earlier stages of CKD (stages 1 to 4), which are estimated to affect 13.1% of the population nationwide or 26.3 million in the United States.

Etiology and Pathophysiology

Progressive destruction of kidney nephrons; GFR will drop gradually, and plasma Cr values will approximately double, with 50% reduction in GFR and 75% loss of functioning nephrons mass. Hyperkalemia usually develops when GFR falls to <20 to 25 mL/min. Anemia develops from decreased renal synthesis of erythropoietin.

Renal parenchymal/glomerularNephritic: hematuria, RBC casts, HTN, variable proteinuria

Focal proliferative: IgA nephropathy, systemic lupus erythematosus (SLE), Henoch-Schönlein purpura, Alport syndrome, proliferative glomerulonephritis, crescenteric glomerulonephritis

Diffuse proliferative: membranoproliferative glomerulonephritis, SLE, cryoglobulinemia, rapidly progressive glomerulonephritis (RPGN), Goodpasture syndrome

Nephrotic: proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia, and edema

Minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis

Amyloidosis, diabetic nephropathy

Vascular: HTN, thrombotic microangiopathies, vasculitis (Wegener), scleroderma

Interstitial tubular: infections, obstruction, toxins, allergic interstitial nephritis, multiple myeloma, connective tissue disease, cystic disease

Postrenal: obstruction (benign prostatic hyperplasia [BPH]), neoplasm, neurogenic bladder

Genetics

Alport syndrome, Fabry disease, sickle cell anemia, SLE, and autosomal dominant polycystic kidney disease can lead to CKD.

Polymorphisms in gene that encodes for podocyte nonmuscle myosin IIA are more common in African Americans than Caucasians and appear to increase risk for nondiabetic ESRD.

Risk Factors

Type 1 or 2 diabetes mellitus (DM); most common

Age >60 years

Cardiovascular disease (CVD) (e.g., HTN [common], renal artery stenosis, atheroemboli)

Previous kidney transplant

Urinary tract obstruction (e.g., BPH)

Autoimmune disease, vasculitis/connective tissue disorder

Family history of CKD

Nephrotoxic drugs (lithium, salicylate, high-dose or chronic NSAIDs, sulfonamide)

Congenital anomalies, obstructive uropathy, renal aplasia/hypoplasia/dysplasia, reflux nephropathy

Hyperlipidemia

Low income/education/ethnic minority status

Obesity/smoking/heroin use

Chronic infection (hepatitis B, hepatitis C, HIV)

General Prevention

Treat reversible causes: hypovolemia, infections, diuretics, drugs (NSAIDs, aminoglycosides, IV contrast).

Treat risk factors: DM, HTN, hyperlipidemia, smoking, and obesity; adjust medication doses to prevent renal toxicity.

Commonly Associated Conditions

HTN, DM, CVD

Diagnosis

History

Patients with CKD stages 1 to 3 are usually asymptomatic; can present with

Oliguria, nocturia, polyuria, hematuria, change in urinary frequency

Bone disease

Edema, HTN, dyspnea

Fatigue, depression, weakness

Pruritus, ecchymosis

Metallic taste in mouth, anorexia, nausea, vomiting

Hyperlipidemia, claudication, restless legs

Erectile dysfunction, decrease libido, amenorrhea

Physical Exam

Volume status (pallor, BP/orthostatic; edema; jugular venous distention; weight)

Skin: sallow complexion, uremic frost

Ammonia-like odor (uremic fetor)

Cardiovascular: Assess for murmurs, bruits, pericarditis.

Chest: pleural effusion

Rectal: enlarged prostate

CNS: asterixis, confusion, seizures, coma, peripheral neuropathy

Diagnostic Tests & Interpretation

Initial Tests (lab, imaging)

GFR can be estimated using the Modification of Diet in Renal Disease (MDRD) and Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) equations. A recent meta-analysis found that MDRD has greater accuracy at GFR 60, whereas the CKD-EPI is more accurate at GFR >60 (1)[A].

Cr clearance (CrCl) can be calculated using Cockcroft-Gault formula to determine medication adjustments.

Urine analysis to assess for evidence of damage

Urine microscopy: WBC casts in pyelonephritis, RBC casts in glomerulonephritis/vasculitis

Urine electrolytes: sodium, Cr, urea (if on loop diuretics)

Albuminuria is more sensitive than proteinuria at detecting disease (2)[B]. Meta-analyses link CVD mortality with albuminuria (2)[A].

Report as a ratio of albumin concentration to Cr concentration (mg/mmol or mg/g)

Ultrasound (initial imaging test of choice): small, echogenic kidneys; may see obstruction (e.g., hydronephrosis); cysts; kidneys may be enlarged with HIV and diabetic nephropathy.

Doppler ultrasound to assess for renovascular disease, thrombosis

Noncontrast CT scan: obstruction, calculi, cysts, neoplasm, renal artery stenosis

MRI/MRA: Avoid gadolinium because of the risk of nephrogenic systemic fibrosis.

Renal arteriogram for renal artery stenosis can be therapeutic (angioplasty or stenting).

Renal scan to screen for differential function between kidneys

Retrograde pyelogram: if strong suspicion for obstruction despite negative finding on ultrasound

Follow-Up Tests & Special Considerations
Additional evaluation may be indicated to assess for complications or cause, as clinically indicated:

Hematology: normochromic, normocytic anemia; increased bleeding time

Chemistry: elevated BUN, Cr, hyperkalemia, metabolic acidosis, increased PTH, HLD, hyperphosphatemia, decreased 25-(OH) vitamin D, hypocalcemia, decreased albumin

Serology: antinuclear antibody (ANA); double-stranded DNA, antineutrophil cytoplasmic antibody; complements (C3, C4, CH50); anti-glomerular basement membrane (GBM) antibodies; hepatitis B, C; and HIV screening

Serum and urine immunoelectrophoresis

Follow-up tests and monitoring:Monitoring the parameters with frequency based on GFR and risk of progression:

Urine albumin and GFR at least annually

Hb: clinically indicated for GFR ≥60, annually for 30 to 59, twice per year for <30 (3)[B]

Calcium, phosphate, PTH, alkaline phosphate actively beginning at CKD stage G3a (4)[C]

25(OH)D (calcidiol) levels with repeated testing determined by baseline values and therapeutic interventions (4)[C]

Therapeutic decisions should be based on trends rather than on a single laboratory value, taking into account all available CKD-MBD assessments (4)[C].

ALERT
Drugs that may alter lab result:

Cimetidine: inhibits Cr tubular secretion

Trimethoprim: inhibits Cr and K+ secretion and may cause/worsen hyperkalemia

Cefoxitin and flucytosine: increases serum Cr

Diltiazem and verapamil (like ACE/ARBs) have significant antiproteinuric effects in patients with CKD.

Diagnostic Procedures/Other
Biopsy: hematuria, proteinuria, acute/progressive renal failure, nephritic or nephrotic syndrome

Treatment

General Measures

Lowering salt intake to <2 g/day of sodium in adults, unless contraindicated (5)[C]

Minimize radiocontrast exposure; prehydrate; N-acetylcysteine use is controversial. Avoid nephrotoxins (NSAIDs, aminoglycosides, etc.).

Encourage smoking cessation, encourage weight loss (if applicable), and limit alcohol consumption (5)[C].

Protein restriction to 0.8 g/kg/day is recommended in CKD G4 to G5 (2)[B]. CKD at risk of progression should avoid dietary protein >1.3 g/kg/day to avoid accelerating progression (2)[B].

Medication

HTN: Goal in adults is BP <130/80 mm Hg if urine albumin excretion is ≥30 mg/24 hr and <140/90 mm Hg if urine albumin excretion is <30 mg/24 hr. Goal in children is <90th percentile for age, sex, weight (5)[B].

ACE-I or ARB recommended for diabetic and nondiabetic adults with albumin excretion >30 mg/24 hr based on evidence of reductions in proteinuria, improved CVD outcomes, and decreased progression of CKD (5)[A]. Monitor potassium and serum Cr (tolerate up to 30% rise unless hyperkalemia develops).

Additional antihypertensive agents should be selected based on the type of CKD and comorbid factors.

Secondary hyperparathyroidism

For GFR <45, monitor for hyperphosphatemia, hypocalcemia, and vitamin D deficiency if intact PTH is elevated beyond lab normals (2)[C].

Cinacalcet, paricalcitol (decrease PTH levels)

Hyperphosphatemia: Maintain phosphate according to reference lab normals (2)[C]. Recommended serum phosphate maintenance levels for CKD patients:Stages 3 to 5 CKD (not on dialysis): Restrict dietary phosphate to 800 to 1,000 mg/day.

Calcium-containing phosphate binders (with meals): calcium carbonate, calcium acetate (risk of hypercalcemia)

Noncalcium phosphate binders (with meals): sevelamer, lanthanum

Vitamin D: inactive vitamin D 25 (ergocalciferol or cholecalciferol), calcitriol (active vitamin D 1,25 [OH]): Vitamin D may increase absorption of phosphate by intestines and should not be started until serum phosphate concentration is controlled.

Anemia: Hb <13 g/dL in adult males or <12 g/dL in adult females. Treat with iron replacement therapy with or without erythropoietin-stimulating agents (ESAs) (3)[B]. Consider ESA if Hb >9 g/dL and <10 g/dL. ESA initiation not recommended for Hb >10 g/dL. If using ESA, goal Hb range 10 to 11 g/dL, not to exceed 11.5 g/dL (3)[B].

Hyperlipidemia: Statins with low-density lipoprotein (LDL) goal is similar to coronary heart disease patients (LDL <70 to 100).

Glycemic control: Target for HbA1c should be adjusted based on risk of hypoglycemia, comorbid conditions, and life expectancy (2)[B]. HbA1c may be falsely low in patients with decreased RBC; glucose logs may be more accurate reflection of glycemic control (2)[C]. Metformin use should be reviewed for GFR between 30 and 44 and discontinued if GFR <30 mL/min/1.73 m2 (2)[C].

Metabolic acidosis: Start treatment when bicarbonate <22 mEq/L with goal to maintain in normal range (2)[C].

Issues For Referral

Nephrology consult: GFR <15: immediate

GFR 15 to 29: urgent

GFR 30 to 59: nonurgent referral

GFR 60 to 89: not required unless with comorbidities

Renal replacement: Prepare for dialysis or transplant when GFR <30 mL/min/1.73 m2.

Surgery/Other Procedures

Placement of dialysis access or transplantation

Inpatient Considerations

Uremia: nausea/vomiting, fluid overload, pericarditis, uremic encephalopathy, resistant HTN, hyperkalemia, metabolic acidosis, hyperphosphatemia

Ongoing Care

Diet

Nutrition consult for CKD diet (2)[C]

Vaccines:

Annual influenza vaccine unless contraindicated (2)

Polyvalent pneumococcal vaccine if GFR <30 mL/min/1.73 m2 and those at high risk of pneumococcal infection (2)

Hepatitis B vaccine with serologic confirmation if high risk of CKD progression and GFR <30 mL/min/1.73 m2 (2)

Clinical Pearls

CKD is defined based on >3 months of kidney functional or structural abnormalities and classified based on GFR and albuminuria.

ACE-I and ARB are first line for HTN treatment in CKD with albuminuria.

Care should be taken in prescribing medication in CKD due to reduced renal clearance of certain medications.

Consider nonurgent nephrologist referral for GFR ≤59 and urgent nephrologist referral for GFR ≤29.

Prognosis

Risk of progression and complications is based on cause, GFR category, albuminuria category, and comorbid conditions (2)[B]. Progression defined as decline in GFR category with 25% decrease in GFR from baseline (2). Rapid progression is decrease in GFR by >5 mL/min/1.73 m2/year (2). Patients with CKD gradually progress to ESRD, with bad prognoses. 5-year survival rate for U.S. patients on dialysis is ~35%.

Complications

HTN, anemia, secondary hyperparathyroidism, renal osteodystrophy, sleep disturbances, infections, malnutrition, electrolyte imbalances, platelet dysfunction/bleeding, pseudogout, gout, metabolic calcification, sexual dysfunction

Answer 3

Describe?

Acute glomerulonephritis (GN) is an inflammatory process involving the glomerulus (Remove waste, excess electrolytes and fluid) of the kidney, resulting in a clinical syndrome consisting of hematuria, proteinuria, and renal insufficiency, often in association with hypertension and edema.

S/sx

Patients may report cola- or tea-colored foamy urine and decreased urine volume.

Edema occurs in many patients, typically in face and lower extremities.

Shortness of breath may occur with significant fluid overload.

Generalized malaise

Causes of Acute GN

• infection such as bacterial endocarditis
• immune disease: lupus, good pastures if IgA nephrpathy, vasculitis (secondary to systemic infection or inflammatory disease
• Infection-related GN (also postinfectious GN)
• BONUS (Can also occur as a result of other bacterial infections, such as infective endocarditis or shunt nephritis, or less commonly with viral or parasitic infections

IgA nephropathy/Henoch-Schönlein purpura (HSP)

Antiglomerular basement membrane disease (anti-GBM disease)

Antineutrophil cytoplasmic antibody (ANCA)-associated GN

Membranoproliferative GN (MPGN)

Lupus nephritis

vasculitis

Cryoglobulin-associated GN)

Infection-related GN is found how longer after resolution of group A β-hemolytic Streptococcus infection

Most commonly manifests 1-2 weeks after resolution of group A β-hemolytic Streptococcus infection

How severe?

Clinical severity ranges from asymptomatic microscopic or gross hematuria to a rapid loss of kidney function over days to weeks, termed rapidly progressive GN (RPGN).

DO NOT MISS THIS
Urgent investigation and treatment are required to avoid irreversible loss of kidney function.

Can cause Goodpasture disease, a notable cause of the pulmonary–renal syndrome

Epidemiology?

In general, systemic and/or local immune activation causes glomerular injury.

Immune-complex mediated: from antigen–antibody formation and

Risk Factors

Epidemics of nephritogenic strains of streptococci are triggers for postinfectious GN.

Anti-GBM disease has been associated with prior pulmonary injury and inhalation exposures, such as hydrocarbon solvents.

ANCA-associated GN may be drug induced (e.g., hydralazine, levamisole-contaminated cocaine) and is also associated with environmental exposures such as silica.

Infection with hepatitis B or C is associated with MPGN.

Infection with hepatitis C is a risk factor for developing cryoglobulinemic GN.

Mutations in alternate complement pathway genes are associated with increased risk of developing complement-mediated Membranoproliferative GN (MPGN)

Onset

Poststreptococcal GN typically occurs 1 to 3 weeks after pharyngitis or 2 to 6 weeks after skin infection.

IgA nephropathy may present within several days after an acute infection.

Joint pain or rash in lupus nephritis

Hemoptysis in pulmonary–renal syndromes (see “Physical Exam”)

Sinusitis, pulmonary infiltrates, arthralgias in ANCA-associated GN

Abdominal or joint pain and purpura in IgA–HSP

Purpura and skin vasculitis in cryoglobulinemia-associated GN

Physical Exam

Majority of patients will have normal exam, but can often present with hypertension and signs of fluid overload.

Sinus disease: often with ANCA-associated GN/GPA

Pharyngitis or impetigo: postinfectious GN or IgA nephropathy

Pulmonary hemorrhage (pulmonary–renal syndrome): anti-GBM disease/Goodpasture, ANCA-associated GN, or lupus nephritis

Hepatomegaly or liver tenderness could point to cryoglobulinemia-associated GN or IgA nephropathy.

Purpura may point to ANCA-associated GN or HSP/IgA nephropathy.

Initial Tests (lab, imaging)

Urinalysis with examination of sediment

Dysmorphic RBCs or RBC casts on urine microscopy indicate glomerular hematuria and strongly suggest the diagnosis of an acute GN.

Pyuria and white blood cell casts may also be present.

Proteinuria: 24-hour collection or random urine protein/creatinine ratio

Can be mild to severe proteinuria, occasionally nephrotic range

Electrolytes, BUN, creatinine, CBC
Test Interpretation

Renal biopsy in peds

If clinical picture is consistent with postinfectious GN in a child, a biopsy may not be required.

If there is clinical suspicion for other causes of acute GN, renal biopsy should be done

Treatment/goal

manage underlying cause and protect the kidneys

Medication/First Line/Hypertension

Diuretics are useful for management of salt retention and edema.

Calcium channel blockers

Avoid ACE inhibitors or ARBs if acute renal dysfunction is present

Medication/First Line/Peripheral edema: Loop diuretics are often required due to the degree of edema.

Pulmonary edema: oxygen and diuretics

INfection?: antimicrobials

Inflammation? corticosteroids; immune suppressing-drugs

Complement/AB deposition? plasmapheresis

Excess fluid/electrolytes no responsive to meds: dialysis

What follow up?

Regular BP checks and urinalysis to detect recurrence,

assessment of renal function to detect acute or follow chronic renal disease as a result of the primary event, and

regular clinical assessment to detect suspicious symptoms that may herald a recurrence (i.e., rash, joint complaint, hemoptysis)

Periodic reassessment of serology tests to follow asymptomatic individuals

Diet No-added-salt diet and fluid restriction until edema and hypertension clear Avoid high-potassium foods if significant renal dysfunction is present. Avoid a high-protein diet.

What are some Complications?

Hypertensive retinopathy and encephalopathy

Microscopic hematuria may persist for years.

Chronic kidney disease

Nephrotic syndrome (~10%)

Answer 4

Epidemiology

Increases with age (median age at diagnosis is 73 years) (1)

More common in Caucasians than in Asians or African Americans

Male > female (4:1); but in smokers, risk is 1:1.

Etiology and Pathophysiology

70–80% is nonmuscle invasive (in lamina propria or mucosa):

What are the Risk Factors?

• Smoking is the single greatest risk factor (increases risk 4-fold) and increases risk equally for men and women (2).
• Use of pioglitazone for >1 year may be associated with an increased risk of bladder cancer. The risk seems to increase with duration of therapy and may also be present with other thiazolidinediones.
• Occupational carcinogens in dye, rubber, paint, plastics, metal, carbon black dust, and automotive exhaust
• Schistosomiasis in Mediterranean (squamous cell) cancer
• Arsenic in well water
• History of pelvic irradiation
• Chronic lower UTI
• Chronic indwelling urinary catheter
• Cyclophosphamide exposure
• High-fat diet

Coffee consumption associated with reduced risk (RR 0.83; 95% CI 0.73–0.94)

DO NOT MISS
A_ny patient who smokes and presents with microscopic or gross hematuria or irritative voiding symptoms such as urgency and frequency not clearly due to UTI should be evaluated by cystoscopy for the presence of a bladder neoplasm._

s/sX

• Painless hematuria is the most common symptom.
• Urinary symptoms (frequency, urgency)
• Abdominal or pelvic pain in advanced disease
• Exposures (see “Risk Factors”)

Physical Exam

Normal in early cases, pelvic or abdominal mass in advanced disease, wasting in systemic disease

Initial Tests (lab, imaging)

• Urinalysis is the initial test in patients presenting with gross hematuria or urinary symptoms such as frequency, urgency, and dysuria.
• Urine cytology (Consult your local lab for volume needed and proper fixative/handling.)
• Cystoscopy with biopsy is the gold standard for at-risk patients with painless hematuria.
• Macroscopic hematuria (55% sensitivity, positive predictive value

Treatment

For nonmuscle-invasive bladder cancer, the treatment is generally removal via cystoscopic surgery For muscle-invasive cancer, a radical cystectomy with pelvic lymphadenectomy is preferred.

Answer 6

What is urinary incontinence?

Urinary incontinence: involuntary loss of urine

What are the 6 types of incontinence?

Stress incontinence: associated with increased intra-abdominal pressure, such as coughing, laughing, sneezing, or exertion

Urge incontinence: sudden uncontrollable loss of urine, preceded or accompanied by urgency, or a sudden compelling desire to urinate that is difficult to delay. Urge incontinence may be associated with overactive bladder or detrusor overactivity.

Mixed incontinence: loss of urine from a combination of stress and urge incontinence

Overflow incontinence: high residual or chronic urinary retention leading to urinary spillage from an overdistended bladder

Functional incontinence: loss of urine due to deficits of cognition and/or mobility

Total incontinence: continuous leakage of urine; leakage without awareness

Epidemiology

Overall prevalence—38% of women age >60 years. A 2012 survey showed stress incontinence affected 37.5% of women age 30 to 50 years (1).

Prevalence in women >75 years is 75%, and 6% of nursing home admissions are directly attributable to incontinence.

Etiology and Pathophysiology of Stress incontinence:

occurs with increased intra-abdominal pressure. Two types:

• Anatomic: due to urethral hypermobility from lack of pelvic support
• Intrinsic sphincter deficiency (ISD): impaired closure of urethra. Urethral mucosal seal and inherent closure from collagen, fibroelastic tissue, and smooth and striated muscles may be lost secondary to surgical scarring, radiation, or hormonal and age-related changes.

Urge incontinence?:

may be due to detrusor overactivity or may be idiopathic

Overflow incontinence:

urinary retention (usually from neurogenic bladder)

Total incontinence:

constant loss of urine. Ectopic ureters in females usually open in the urethra distal to the sphincter or in the vagina, causing continuous leakage; may also occur with fistulous connections between bladder, ureters, or urethra and vagina or uterus

Women with urge urinary incontinence report poorer quality of life than those with stress incontinence .

Risk Factors

• Advanced age,
• impaired functional status, obesity (BMI >30),
• history of gestational diabetes,
• pregnancy,
• vaginal childbirth,
• pelvic surgery or radiation,
• urethral diverticula,
• genital prolapse,
• smoking,
• chronic obstructive pulmonary disease (COPD),
• cognitive impairment,
• constipation,
• caffeine
• pelvic floor dysfunction

General Prevention

• Obesity and caffeine avoidance, smoking cessation, high-fiber diet to reduce constipation

Commonly Associated Conditions

Pelvic organ prolapse, UTI, COPD, diabetes mellitus, neurologic disease, obesity, chronic constipation, depression, low libido, dyspareunia, and any disease that results in chronic cough

Diagnosis

History

Important to screen for symptoms because only 45% of women who reported at least twice weekly urine leakage on a U.S. survey sought care for their symptoms (2)

Age: Stress incontinence is more common in women aged 19 to 64 years, whereas mixed incontinence is more common in women >65 years. Onset from childhood indicates congenital causes (e.g., ectopic ureter).

Amount and frequency of leakage; pad usage

Stress incontinence: occurs in small spurts; patients typically remain dry at night in bed.

Urge incontinence: sudden urge followed by leakage of large amounts, usually associated with frequency and nocturia. Sensory stimuli may trigger (e.g., cold).

Continuous slow leakage in between regular voiding indicates ectopic ureter or urinary fistula.

Pain: Suprapubic pain with dysuria implies urinary infection or interstitial cystitis.

Medical history

• Neurologic conditions or suggestive symptomatology: cerebrovascular accident, parkinsonism, multiple sclerosis, myelodysplasia, diabetes, spinal cord injury
• Radiation to pelvic and vaginal areas: causes ISD, overactive bladder, fibrotic changes of pelvic floor musculature, and low bladder compliance
• Obstetric history: Weakness of the pelvic floor is more likely in multiparous women.
• History of smoking and COPD with a chronic cough can aggravate incontinence.
• Constipation can aggravate incontinence.
• Surgical history: Pelvic surgery, including gynecologic and bowel surgery, can injure the pelvic floor musculature and affect neurologic function.

Medications

Sympatholytic α-blockers (terazosin, prazosin, doxazosin, tamsulosin, alfuzosin, silodosin) can cause or worsen incontinence.

Medication that can cause Retention with overflow incontinence?Sympathomimetic agents, tricyclic antidepressants, anticholinergics, and opioids can cause retention with overflow incontinence.

Physical Exam

• Obesity (BMI)
• General neurologic examination
• Mental status, speech, intellectual performance
• Motor status: gait, generalized or focal weakness, rigidity, tremor
• Sensory status: impairment of perineal–sacral area sensation
• Urologic examination
• Abdomen: masses, incisional scars of previous surgeries
• Suprapubic tenderness: may indicate cystitis
• Palpable, distended bladder: chronic urinary retention

Pelvic examination

• Examination of the perineum and external genitalia, including tissue quality and sensation
• Vaginal (half-speculum) examination for prolapse
• Bimanual pelvic and anorectal examination for pelvic masses, fecal impaction, pelvic floor function, and so forth
• Assessment of pelvic floor resting tone and function (ability to isolate and contract pelvic floor musculature) (3); can use Oxford scale to grade strength
• Urethral mobility (cotton swab test): displacement angle of urethra-bladder neck at least 30 degrees from horizontal with Valsalva (2)
• Stress test: positive with involuntary loss of urine from urethral meatus with cough or Valsalva maneuver. If test is negative in supine position, can try in standing position. Ensure that patient has a comfortably full bladder (4). Test has 98% positive predictive value for SUI (3).
• Cystocele: if evident, should stage (grade 0 to 4)
• Rectocele: if evident, should stage (stage 0 to 4)

Diagnostic Tests & Interpretation

• Urinalysis and urine culture
• Renal function assessment: recommended if renal impairment is suspected
• Imaging is unnecessary in uncomplicated patients.
• Bladder scan to evaluate postvoid residual (PVR) if overflow suspected (>100 mL) (5)
• TSH if constipation is present
• Upper tract imaging if upper tract involvement is suspected: renal ultrasound

Diagnostic Procedures/Other

Urodynamic studies and cystoscopy are not indicated in initial workup and should only be performed after failing conservative treatment; this includes cystometric study of detrusor function and pressure flow studies looking at bladder emptying (1,5)[B].

Cystoscopy should be performed in women with microscopic hematuria and may be helpful in evaluating recurrent UTIs (3).

Results of urodynamic testing are not predictive of treatment success (2)[A] and are not necessary prior to surgery for uncomplicated patients with known SUI (3)[C].

Treatment

General Measures

• Treat correctable causes (e.g., UTI).
• Encourage weight loss in obese patients.
• Aggressively correct constipation.
• Treat mixed for primary symptom type (5)[C].

Medication

Urge incontinence: anticholinergic agents (inhibit involuntary detrusor contractions) (1)[A]

• Tolterodine (Detrol LA): 2 to 4 mg/day PO
• Oxybutynin (Ditropan XL): 5 to 15 mg/day PO
• Solifenacin (VESIcare): 5 to 10 mg/day PO
• Darifenacin (Enablex): 7.5 to 15.0 mg/day PO
• Trospium chloride (Sanctura XR): 20 to 60 mg/day PO—does not cross blood–brain barrier (3)
• Transdermal oxybutynin gel (Gelnique): 10%, 1 g applied daily
• Transdermal oxybutynin patch (Oxytrol): twice weekly—available over the counter (OTC)
• Fesoterodine (Toviaz): 4 to 8 mg/day PO
• Fesoterodine may be more effective than tolterodine, at the expense of greater adverse effects (1)[B].
• Mirabegron: alternative to anticholinergics.

No single agent has been shown to be overall superior (5).

Extended-release and transdermal medications cause fewer side effects (1)[C].

Dry mouth, dry eyes, constipation, impaired cognitive function, and other anticholinergic side effects can limit use.

Higher doses are more effective but have higher risk of side effects (4)[B].

IMPORTANT PRECSUTIONS:

Avoid with narrow-angle glaucoma, urinary retention (PVR >250 mL), impaired gastric emptying, frail elders (3); may worsen existing cardiac arrhythmias (1)

Third Line
Stress incontinence

Duloxetine (Cymbalta) 40 mg is effective but causes GI and CNS side effects; no differences between SUI and MUI (5)[A]

Estrogen may be beneficial in topical form for symptoms of urgency and frequency in postmenopausal women with vaginal atrophy, but transdermal or PO estrogen may worsen symptoms (1)[B],(2)[C].

First Line

• Lifestyle changes:
• Reduce BMI to <25; can reduce weekly incontinence episodes by 28–47% (2)[A]. Even moderate weight loss (5–10%) can help (6)[A].
• Bladder diaries (fluid intake, voids, leakage)
• Decrease fluid intake before bedtime.
• Reduce caffeine to <1 cup coffee per day (2)[B].
• Aggressive treatment of constipation: Limit medications that may induce constipation. Treat constipation with polyethylene glycol 3350 (PEG 3350), increased fluid intake, and nutrition (5)[C].
• Pelvic floor muscle training with Kegel exercises may be used alone or in combination with bladder training, biofeedback, or electrical stimulation (2).

Proper technique should be confirmed on exam by trained physical therapists. Recommend 3 sets of 10 contractions held for 10 seconds each (1)[C].

Women who undergo pelvic floor muscle training are 8 times more likely to report cure than with no treatment (6)[A].

Bladder training:

Scheduled voiding, urge suppression between voids

No differences in treatment efficacy by type of incontinence so reasonable to start with lifestyle changes in all types (2)[A]

Second Line
Stress incontinenceSurgical management for stress incontinence

Mesh midurethral sling (most common, most studied surgical intervention) (2)[C],(4)[A]

Women with moderate to severe stress incontinence have better outcomes at 1 year with midurethral slings than pelvic floor muscle training (2)[A].

Main approaches with similar effectiveness: retropubic (more perioperative complications) versus transobturator (more groin pain) (2,4)[A]

Autologous fascial bladder neck slings should be considered in severe incontinence and fixed urethra, urethral diverticula or fistula, or with complications from previously placed mesh (2)[C].

Pelvic organ prolapse may unmask incontinence in up to 40% of women; consider repair of both during same surgery (2)[A].

Periurethral bulking agents (silicone polymers, collagen) can increase periurethral resistance in women who have recurrent symptoms after surgery or who cannot tolerate surgery. However, they are 2 to 5 times less effective than surgery and often require repeat injections (2)[A].

Occlusive and supportive devices (e.g., cones, pessaries) are a low risk alternative to surgery (4,5,6)[C].

Acupuncture (1)[B]

Urge incontinence

Intradetrusor onabotulinumtoxinA 100 to 200 U (urinary retention common, temporary self-catheterization may be needed) (5)[A]

Sacral nerve stimulation: 61% of patients found this treatment effective and efficacy maintained at mean 30 months; invasive with frequent complications (3)[B]

Posterior tibial nerve stimulation: office-based therapy, requires frequent visits (3)[B]

Bladder augmentation: At average 6-year follow-up, only 53% were continent (5)[B].

Geriatric Considerations
Anticholinergics (oxybutynin, in particular) can worsen cognition and delirium; the effects are cumulative and increase with length of exposure (5).

β3 Agonist (leads to detrusor muscle relaxation and increased bladder capacity): mirabegron (Myrbetriq ER): 25 to 50 mg/day PO (1)[B]; onset of action delayed ~8 weeks; increases BP (avoid use in those with uncontrolled HTN, end-stage renal disease, or significant liver impairment); safe in geriatric patients (5); recommend BP check 2 weeks after starting (3)[C].

Can consider dual therapy with mirabegron and low-dose anticholinergics (3,5)

Ongoing Care

Follow-up Recommendations

Patient Monitoring
Periodic long-term follow-up with outcome-based questionnaire surveys

Patient Education

Instructions on self-care and warning signs are available at PubMed Health: Urinary incontinence: https://medlineplus.gov/urinaryincontinence.html.

Prognosis

Significant improvements are usually obtained with most patients.

Complications

Prolonged exposure to urine causes skin breakdown and dermatitis, which may lead to ulceration and secondary infection.

Inability to self-care (including toileting) is the precipitating factor for many nursing home admissions.

Increased risk for falls

Social isolation/depression

Weight gain (due to self-limiting exercise from fear of leakage)

Impaired sexual function

Impaired quality of life

Additional Reading

Gormley EA, Lightner DJ, Burgio KL, et al. Diagnosis and treatment of overactive bladder (non-neurogenic) in adults: AUA/SUFU guideline. J Urol. 2012;188(Suppl 6):2455–2563. [PMID:23098785]

Riemsma R, Hagen S, Kirschner-Hermanns R, et al. Can incontinence be cured? A systematic review of cure rates. BMC Med. 2017;15(1):63. [PMID:28335792]

Smith A, Bevan D, Douglas HR, et al. Management of urinary incontinence in women: summary of updated NICE guidance. BMJ. 2013;347:f5170. [PMID:24021756]

Codes

ICD-10

N39.3 Stress incontinence (female) (male)

N39.41 Urge incontinence

N39.42 Incontinence without sensory awareness

N39.45 Continuous leakage

N39.46 Mixed incontinence

N39.490 Overflow incontinence

N39.498 Other specified urinary incontinence

R32 Unspecified urinary incontinence

ICD-9

625. 6 Stress incontinence, female
626. 30 Urinary incontinence, unspecified
627. 31 Urge incontinence
628. 33 Mixed incontinence (male) (female)
629. 34 Incontinence without sensory awareness
630. 37 Continuous leakage
631. 38 Overflow incontinence
632. 91 Functional urinary incontinence

SNOMED

129847007 Functional urinary incontinence

129853007 Total urinary incontinence

165232002 urinary incontinence (finding)

397878005 Overflow incontinence of urine

413343005 Mixed incontinence

60241006 Female urinary stress incontinence (finding)

87557004 Urge incontinence of urine (finding)

Clinical Pearls

Rule out infection (UTI or STI) and hematuria.

Aggressively treat constipation.

Try lifestyle changes first for all types of urinary incontinence.

If lifestyle changes do not work for stress incontinence, mesh midurethral sling surgery has high success rates.

If lifestyles changes do not work for urge incontinence, anticholinergic medications and/or mirabegron should be trialed.

Answer 7

Urolithiasis–Description

Stone formation within the urinary tract: Urinary crystals bind to form a nidus which grows to form a calculus (stone).

populations with Increased incidence in

patients with surgically induced absorption issues, such as Crohn disease and gastric bypass surgery

Etiology and Pathophysiology

• Supersaturation and dehydration lead to high salt content in urine which congregates.
• Stasis of urine
• Renal malformation (e.g., horseshoe kidney, ureteropelvic junction obstruction)
• Incomplete bladder emptying (e.g., neurogenic bladder, prostate enlargement, multiple sclerosis)
• Crystals may form in pure solutions (homogeneous) or on existing surfaces, such as other crystals or cellular debris (heterogeneous).
• Calcium oxalate and/or phosphate stones (80%)Hypercalciuria
• Absorptive hypercalciuria: increased jejunal calcium absorption
• Renal leak: increased calcium excretion from renal proximal tubule
• Resorptive hypercalciuria: mild hyperparathyroidism
• Hypercalcemia
• Hyperparathyroidism
• Sarcoidosis
• Malignancy
• Immobilization
• Paget disease

HyperoxaluriaEnteric hyperoxaluria

Intestinal malabsorptive state associated with irritable bowel disease, celiac sprue, or intestinal resection

Bile salt malabsorption leads to formation of calcium soaps.

Primary hyperoxaluria: autosomal recessive, types I and II

Dietary hyperoxaluria: overindulgence in oxalate-rich food

Hyperuricosuria

Seen in 10% of calcium stone formers

Caused by increased dietary purine intake, systemic acidosis, myeloproliferative diseases, gout, chemotherapy, Lesch-Nyhan syndrome

Thiazides, probenecid

Hypocitraturia

Caused by acidosis: renal tubular acidosis, malabsorption, thiazides, enalapril, excessive dietary protein, topiramate, indinavir

Stone types

• Uric acid stones (10–15%): hyperuricemia causes as discussed earlier
• Struvite stones (5–10%): infected urine with urease-producing organisms (most commonly Proteus sp.)
• Cystine stones (<1%): autosomal recessive disorder of renal tubular reabsorption of cystine
• Bladder stones: seen with chronic bladder catheterization and some medications (indinavir)
• In children: usually due to malnutrition

Risk Factors

• White > African American in regions with both populations
• Family history
• Previous history of nephrolithiasis
• Diet rich in protein, refined carbohydrates, and sodium; carbonated drinks
• Occupations associated with a sedentary lifestyle or with a hot, dry workplace
• Incidence rates peak during summer secondary to dehydration.
• Obesity
• Surgically/medically induced malabsorption (Crohn disease, gastric bypass, celiac)
• General Prevention
• Hydration (3)[A]
• Decrease salt and meat intake.
• Avoid oxalate-rich foods.

Pregnancy Considerations

• Pregnant women have the same incidence of renal colic as do nonpregnant women.
• Most symptomatic stones occur during the 2nd and 3rd trimesters, heralded by symptoms of flank pain/hematuria.
• Most common differential diagnosis is physiologic hydronephrosis of pregnancy. Use ultrasound to avoid irradiation. Noncontrast-enhanced CT scan also is diagnostic.

Treatment goals

• Control pain, avoid infection, and preserve renal function until birth or stone passage.
• 30% require intervention, such as stent placement.

S/sx

• Pain
• Renal colic: acute onset of severe groin and/or flank pain
• Distal stones may present with referred pain in labia, penile meatus, or testis.
• Microscopic/gross hematuria occurs in 95% of patients.
• Nonspecific symptoms of nausea, vomiting, tachycardia, diaphoresis
• Low-grade fever without signs of infection
• Infectious origin: associated with high-grade fevers require more urgent treatment (see the following text)
• Frequency and dysuria especially occur with stones at the vesicoureteric junction (VUJ).

Asymptomatic: nonobstructing stones within the renal calyces

Physical Exam

Tender costovertebral angle with palpation/percussion and/or iliac fossa

Diagnostic Tests & Interpretation

• Urinalysis for RBCs, leukocytes, nitrates, pH (acidic urine <5.5 is associated with uric acid stones; alkaline >7 with struvite stones)
• Midstream urine for microscopy, culture, and sensitivity
• Blood: urea, creatinine, electrolytes, calcium, and urate; consider CBC.
• Parathyroid hormone only if calcium is elevated
• Stone analysis if/when stone passed

Initial Tests (lab, imaging)

• Noncontrast-enhanced helical CT scan of the abdomen and pelvis has replaced IV pyelogram as the investigation of choice (4)[A].
• Renal ultrasound may be as effective with lower radiation at diagnosis as well as identifying obstruction (5)[B].
• X-ray of kidneys, ureter, and bladder to determine if stone is radiopaque or lucent
• Calcium oxalate/phosphate stones are radiopaque.
• Uric acid stones are radiolucent.
• Staghorn calculi (that fill the shape of the renal calyces) are usually struvite and opaque.
• Cystine stones are faintly opaque (ground-glass appearance).

Ultrasound has low sensitivity and specificity but is often the first choice for pregnant women and children.

Treatment

General Measures: 75% of patients are successfully treated conservatively and pass the stone spontaneously.

Increased fluid intake; eliminate carbonated drinks.

medications that increase risk of stone formation: probenecid, loop diuretics, salicylic acid, salbutamol, indinavir, triamterene, acetazolamide.

Medication

• provide pain medications: Adequate pain control can be achieved with NSAIDs.
• Medical expulsive therapy: α1-Antagonists (e.g., tamsulosin) (6) and calcium channel blockers (e.g., nifedipine) improve likelihood of spontaneous stone passage with a number needed to treat (NNT) of ~5.

Category C in pregnancy

Stones that do not pass usually require surgical intervention.

30–50% of patients will have recurrent stones.

Issues For Referral

Urgent referral of patients with UTI/sepsis or acute renal failure/solitary kidney

Early referral of pregnant patients, large stones (>8 mm), chronic renal failure, children

Refer patients if no passage at 2 to 4 weeks or poorly controlled pain.

Additional Therapies

Uric acid stone dissolution therapy

Alkalinize urine with potassium citrate C; keep pH >6.5.

Allopurinol 100 to 300 mg/day PO (for those who continue to form stones despite alkalinization of urine)

When need Immediate relief of obstruction is required for patients with the following conditions:

Sepsis

Renal failure (obstructed solitary kidney, bilateral obstruction)

Uncontrolled pain, despite adequate analgesia

Emergency surgery for obstruction

Placement of a retrograde stent (i.e., endoscopic surgery, usually requires an anesthetic)

Radiologic placement of a percutaneous nephrostomy tube

Elective surgery for stone treatment

Extracorporeal shock wave lithotripsy

Ureteroscopy with basket extraction/lithotripsy (laser/pneumatic)

Percutaneous nephrolithotomy

Open surgery is uncommon.

Inpatient Considerations

Analgesia

Combination of NSAIDs (ketorolac 30 to 60 mg) and oral opiate

Parenteral opioid if vomiting or if preceding fails to control pain (morphine 5 to 10 mg IV or IM q4h)

Antiemetic if required or prophylactically with parenteral narcotics

Septic patients with urosepsis or pyonephrosis may require IV antibiotics (once blood and urine cultures are taken), IV fluids, and in severe cases cardiorespiratory support in intensive care during recovery.

Ongoing Care

Follow-up Recommendations

• Patients with ureteric stones who are being treated conservatively should be followed until imaging is clear or stone is visibly passed.
• Strain urine and send stone for composition.
• Tamsulosin and nifedipine in selected patients to speed passage
• Present to the hospital if pain worsens/signs of infection.
• If pain management is suboptimal or stone does not progress or pass within 2 to 4 weeks, patient should be referred to a urologist and imaging should be repeated.

Patients with recurrent stone formation should have follow-up with a urologist for metabolic workup: 24-hour urine for volume, pH, creatinine, calcium, cystine, phosphate, oxalate, uric acid, and magnesium.

Education:

• Diet
• Increased fluid intake for life cannot be overemphasized for decreasing recurrence. Encourage intake of 2 to 3 L/day; advise patient to have clear urine rather than yellow.
• Decrease or eliminate carbonated drinks.
• Patients who form calcium stones should minimize high-oxalate foods such as green leafy vegetables, rhubarb, peanuts, chocolates, and beer.
• Decrease protein and salt intake.
• Lowering calcium intake is inadvisable and may even increase urine calcium excretion.
• Increase phytate-rich foods such as natural dietary bran, legumes and beans, and whole cereal.
• Avoid excessive vitamin C and/or vitamin D.

Clinical Pearls

Incidence in industrialized countries seems to be increasing, probably due to improved diagnostics as well as to increasingly rich diets.

Vesical calculosis (bladder stones) due to malnutrition during early life is frequent in Middle East and Asian countries.

Medical expulsive therapy: α1-Antagonists (e.g., terazosin) and calcium channel blockers (e.g., nifedipine) improve likelihood of spontaneous stone passage with NNT of ~5.

Increased fluid intake for life cannot be overemphasized for decreasing recurrence. Encourage 2 to 3 L/day intake; advise patient to have clear urine rather than yellow.

Patients who form calcium stones should minimize high-oxalate foods such as green leafy vegetables, rhubarb, peanuts, chocolates, and beer.

Decrease protein and salt intake.

Lowering calcium intake is inadvisable and may even increase urine calcium excretion.