Renal

Acid-Base Balance

Vomiting VS Diuretics Abuse

• Hypokalemic Hypochloremic Metabolic Alkalosis

• Increase Potassium in Urine

• HIGH sodium in Urine [due to drug effect on inhibiting Na reabsorption in kidney]

• HIGH Chloride in Urine (>20) [due to drug effect on inhibiting Cl reabsorption in kidney]
• LATE ⇒ LOW Chloride in Urine as chloride is depleted

Henderson-Hasselbalch Equation

• pH = 6.1 + log ( [HCO3] / (0.03 x PaCO2 ) )

• So having 2 of the above 3 needed (ph, HCO3, PCO2), we can get the missing one

ABG Interpretation:

Evaluation of Metabolic Acidosis

 

 

• Pancreatic Fistula/Post-op pancreatic leak causes metabolic acidosis due to loss of HCO3 rich fluid
• Arrows would be: LOW pH, LOW, HCO3, and NAGMA.
• PCO2 would compensate by also being LOW

 

• Post-Ictal Metabolic Acidosis is transient & self-limiting.
• Usually resolves after 90 mins, so management is observation & repeat after 2 hours
 

• Bicarb IV administration for metabolic acidosis is indicated only if pH ≤7.1
• As Bicarb causes depressed myocardial functions & increased lactic acid production, so the use above 7.1 has little benefit

 

Ethylene glycol toxicity:

• Sweet-tasting alcohol (causes sweet odor in breath) + CNS sedation + High-anion gap metabolic acidosis + Enveloped Shaped Urine Crystal
• Glycol → glycolate → oxalate → calcium oxalate tubular dysfunction (Enveloped/ Dumbbell-shaped crystals) → AKI

Evaluation of Metabolic Alkalosis

 

• Bartter Syndrome ⇒ Loop-like effect

• Gitelman Syndrome ⇒ Thiazide-like effect

 

 

 

Renal Tubular Acidosis (RTA)

Show Summary

• Type 1 Causes: Sjogren Syndrome

• Type 4
• Also called “Aldosterone Resistance OR Hyperkalemic RTA“
• Impaired function of collecting tubules → Aldosterone can’t exert its actions → can’t excrete K & H and reabsorb Na
• End Result is Hyperkalemia, Metabolic Acidosis, and LOW-normal sodium
• NON-Anion Gap Metabolic Acidosis

Hypermagnesemia

• Common in patients with CKD

• Causes decreased power, sensation, deep tendon reflexes, resp depression, paralysis
• CVS effects: conduction defects, bradycardia, hypotension
• Leads to REFRACTORY:
• Hypocalcemia (due to inhibition of PTH)
• Hypokalemia (due to Renal Outer Medulla K [ROMK] channels, which inhibit K secretion by the presence of intracellular magnesium)
• Low Magnesium ⇒ no ROMK inhibition ⇒ Potassium secretion & refractory hypokalemia

Hypercalcemia

• Primary & Tertiary Hyperparathyroidism

• Sarcoidosis (Erythema Nodosum + Non-productive Cough + Papular sarcoidosis)
Show Pic

• Severe (>14 mg/dL) OR Symptomatic ⇒ Immediate Saline + calcitonin + avoid loops unless HF exists + Longterm bisphosphonate

• Moderate (12-14 mg/dL) ⇒ No immediate treatment + Longterm bisphosphonate

• Asymptomatic/Mild (<12 mg/dL) ⇒ No ttt; avoid thiazides, lithium, dehydration, prolonged bed rest

Hypernatremia

• Is it Euvolemic hypernatremia?
• GIVE Hypotonic Solutions (e.g. 5% dextrose or 0.45% saline)
• Explanation ⇒ We are trying to replace free water with minimal salt, so giving hypotonic solution causes an increase in water levels & prevents increase in sodium levels
 

• Is it Hypovolemic hypernatremia?
• is it Symptomatic?
• No ⇒ GIVE Hypotonic Solutions (e.g. 5% dextrose)
• Yes ⇒ GIVE Isotonic Solutions (e.g. 0.9% saline) until euvolemia
• Then switch to hypotonic solutions

Hyponatremia

 

First Step is excluding “pseudo-hyponatremia”, conditions that increase serum osmolality”

• Hyperglycemia (blood glucose pulls water out of cells → apparent hyponatremia)

• Uremia (urea increases osmolality)

 

2nd Step to see if ADH is working

• Normally Id expect ADH to increase to cause water reabsorption & increased urine osmolality
• IF LOW ⇒ PP, Malnutrition
• IF HIGH ⇒ INTACT ADH ⇒ Step 3

 

Step 3 (look for kidney response):

• Is urinary Na low? ⇒ Volume depletion/CHF/Cirrhosis {LOSS OF Effective Plasma Volume}

• Is urinary Na high?
• SIADH ⇒ INCEASED FREE WATER REABSOPRITON
• AI ⇒ decreased aldosterone
• Hypothyroidism ⇒ Edema & decreased CO

• Management:
• If hypervolemic [Water > Na] ⇒ Diuretics
• If hypovolemic ⇒ No specific ttt (may benefit from Isotonic Saline)
• (CHATGPT added) If Euvolemic hyponatremia (SIADH) ⇒ Diuretics + Fluid Restriction + ttt of cause
 
• If patient is severely hyponatremic (<120) OR if symptomatic (seizures) ⇒ consider hypertonic saline REGARDLESS OF VOLUME STATUS

Hypokalemia

• Patient with COPD + treated with albuterol (beta 2 agonist) caused by Adrenergic agents effects of
• Potassium Shift intracellularly (via stimulating Na/K ATPases)
• Insulin secretion

Hyperkalemia

• Hyperkalemic Emergency:
• Urgent treatment with sodium gluconate OR insulin + glucose is indicated in
• Serum K is >6.5
• Rapid increase in K during tissue breakdown
• Symptomatic Hyperkalemia (ECG changes - Arrhythmias)

• Moderate/Chronic Hyperkalemia
• Low-Potassium Diet
• Avoid Meds that increase K
• Cation Exchange Agent (Patiromer)

Hypophosphatemia

• Chronic alcohol + developed refeeding Syndrome can predispose to hypophosphatemia
• Muscle weakness, hyporeflexia, rhabdomyolysis, hemolysis, arrythmia, CHF

Urine & Serum Disorders

Evaluation of Polyuria

Patient has polyuria:

1. Look at urine osmolality
1. if > 600 ⇒ Think solute diuresis (glucose, mannitol)
2. if <300 ⇒ Think water diuresis (Diabetes Insipidus & Primary Polydipsia)
 

🚨

POLYURIA IS NOT A FEATURE OF SIADH

 

Acute Kidney Injury (AKI)

• Bilateral Renal Vein Thrombosis (Thrombectomy/Thrombolysis)

• Crystal-Induced AKI (Acyclovir)
• ttt → Fluids +/- loops to flush kidney out

• Calcineurin Inhibitors (causes vasoconstriction; ttt → adjust dosing & blood levels)

• Hepatorenal Syndrome (splanchnic VD → decreased EABV → increased RAAS → Renal VC & worsening of Creatinine)
• Causes Metabolic Acidosis & Hyperkalemia (due to impaired renal clearing)
• Can be precipitated by GI bleeds or infections (SBP)
• Only ttt is liver transplantation
Show Dx algorithm?



 

• Rhabdomyolysis
• Can be caused by drugs (Statins, Fibrates, Colchicine, Opioids, Cocaine, Amphetamines, BDZ, Ethanol)
• Causes hyperkalemia & hyperphosphatemia & hypocalcemia

• Acute Kidney Injury + HYPERcalcemia
• This is MM
• AKI causes hypocalcemia, so having hypercalcemia is buzzy for a tumor that increases calcium
• Calcium deposition & Bence-Johns protein ⇒ Intrinsic Renal Injury

• Contrast-Associated AKI
• Presents as worsening of creatinine levels 24-48 hours post exposure
• Later return to baseline within 3-7 days
• Prevention involves increasing hydration (IV saline), avoidance of NSAIDs, and minimize contrast load

Uremia

• Uremic Encephalopathy
• Occurs with advanced Renal Failure (not with creatinine levels of 2-2.5)

• Uremia-Induced Platelet Dysfunction
How?

Glomerulonephritis

Female + Pancytopenia + Fatigue + headache + hx of allergic rhinitis + HTN + Bilateral lower pitting edema + decreased C3

• THINK ⇒ LUPUS NEPHRITIS
• May have associated Discoid Lupus ( A well-defined, erythematous plaque with scale, pigment alteration, and central scarring)
 

URGENT Biopsy is indicated to reach a dx & defines the histological class for ttt. [histological class depends on site of IC deposition]

• Mesengial IC deposition (Class I & II)
• presentation → asymptomatic or microscopic hematuria
• ttt → Close monitoring + ACEi/ARBs for proteinuria

• Subendothelial IC deposition (Class III & IV)
• presentation → GN
• ttt → immunosuppressants & steroids + ACEi/ARBs for proteinuria

• Subepithelial IC deposition (Class V)
• presentation → Nephrotic Syndrome
• ttt → immunosuppressants & steroids + ACEi/ARBs for proteinuria

• ESRD with scarring > 90% (Class VI)
• unlikely to benefit from ttt

Nephrotic Syndrome

Membranous Nephropathy

• BIOPSY ⇒ DIFFUSE THICKENING OF GBM

• Can be idiopathic/primary due to antibodies to endogenous glomerular antigens

• If staining for PLA2R is negative (Primary), look for Secondary Causes:
• However, diagnosis of secondary causes should be excluded (especially in children)
• Infections (HBV, HCV, Syphilis) ⇒ Antibodies & Antigens Screening
• Malignancies ⇒ CT Chest
• Autoimmune Diseases (SLE/Thyroiditis) ⇒ ANA/C1q
• Drugs (NSAIDs, Penicillamine) ⇒ Drug history

Focal Segmental Glomerulosclerosis (FSGS)

• Biopsy Findings: Areas of sclerosis, areas of enlargement with no sclerosis, and podocyte effacement

• Causes:
• Primary (Immune)
• Secondary:
• Hyperfiltration (Obesity, Solitary Kidney, Reflux Nephropathy)
• Podocyte Toxins (Heroin)
• Infections (HIV)
 

• Treatment in general:
• Loops
• ACE inhibitors or ARBs
• PLUS
• HIV-associated nephropathy (ttt → Antiretroviral therapy)
• Severe obesity (ttt → weight loss)

Minimal Change Disease (MCD)

• Pathophysiology: T-cell → release of cytokines → damage of podocytes

Nephritic Syndrome

Membranoproliferative Glomerulonephritis (MPGN)

• Associated with serum cryoglobulins (low C4 & C3) ⇒ Cryoglobulinemia (small vessel vasculitis “palpable purpura + joint pain” & chronic HCV infection)
• HBV/HIV also possible

IgA Nephropathy

• Dark Red Urine 2-3 days post-URT infection

• Normal C3 & C4

PSGN

• Low C & CH50

• Low/Normal C4 levels

• TTT: Loops +/- CCB (if hypertensive encephalopathy or HTN refractory to diuretics)
• ACEis are NOT used as they exacerbate risk of hyperkalemia
• IF MEDICAL TTT FAILS ⇒ Dialysis

Renal Disorders

Analgesics Nephropathy

• Caused by concurrent prolonged usage of Acetaminophen + NSAIDs/Aspirin

• CT shows Renal Papillary Calcification & Irregular Kidney Contours

Acute Interstitial Nephritis

• Management is STOP offending drug +/- steroids (if symptoms persist)

Diabetic Nephropathy

• Detected 5 years after dx of T1DM, but is often present at diagnosis in patients with T2DM

• Urinary Albumin/Creatinine Ratio >30 mg/g suggests DN
• HIGHLY SENSATIVE AT ALL STAGES & SHOULD BE ASSESSED REGULARLY

• Management: SGLT-2 Inhibitors, ACE inhibitor, or ARBs

Rising Creatinine levels

• ACE inhibitors cause a RAPID elevation in Creatinine (within 3-5 days)

• BPH causes a slower elevation in creatinine (over months)
• Obstructive Uropathy is defined as postvoid residual of >50mL
• Do Renal US to exclude for hydronephrosis & other causes of obstruction
• Note: Bilateral obs causes an increase in Creatinine vs Unilateral stones cause no increase in creatinine

• Post-surgery due to pre-renal AKI, secondary to decreased renal perfusion (ttt → Isotonic Saline)

ADPKD

• Drug of Choice for HTN ttt is ⇒ ACE inhibitors

Nephrolithiasis (Kidney Stones)

• Dx → US or CT (NON-CONTRAST)

• Management ALGO:



 

 

Ureterolithiasis:

• ≤5 mm stones ⇒ Pass Spontaneously

• > 5 → ≤10 mm ⇒ Alpha Blockers

• ≥ 10mm ⇒ unlikely to Pass Spontaneously without intervention

 

Uric Stones:

• management: Increase fluid intake + alkalinization of urine (with potassium citrate)

• Prevention of CALCIUM stones
• Increased Fluid Intake (>2L/day)
• Decreased Sodium (increases renal calcium reabsorption, as both Na excretion & Ca reabsorption are linked)
• Increased Citrate (binds urinary calcium → decreases stone formation)
• Increased Potassium “potassium citrate” (increases urinary citrate excretion → binds urinary calcium → decreases stone formation)
• Decreased Animal Proteins (decreased urinary calcium excretion, due to decreased urine acidity → increased citrate → binds calcium)
• SPECIFIC TO CALCIUM OXALATE STONES:
• Adequate calcium intake (1,200 mg/day; causes decreased oxalate absorption in GI)
• Decreased Oxalate (in spinach; decreased urinary oxalate excretion)

Hematuria

• Glomerular
• RBC Casts are diagnostic
• Dysmorphic RBCs are highly specific
• Proteinuria is almost always present ≥1
• Dark Red/Brown Urine
• NO clots
 

• Non-Glomerular:
• NO casts
• NORMAL RBCs (rare)
• Trace/Negative Proteinuria
• Bright Red or Pink
• Possible Clots (Diagnostic)

 

• Long distance running causes hematuria via:
• Benign Bladder trauma/injury from running:
• RBCs + normal CK
• Rhabdomyolysis
• NO RBCs + high CK
• March hemoglobinuria (rare)

Tumors

Renal Cell Carcinoma

• Smoker

• Can present with scrotal varicocele “that fails to empty when the patient is recumbent” due to obstruction of gonadal vein
• If it presents like that, best next step in US of the abdomen (in a child aged 4, it could be caused by Wilm’s Tumor)

• Produces EPO → reactive/2ry polycythemia
• FIRST TEST OF CHOICE ⇒ ABDOMINAL CT
• also used to exclude HCC, which can also produce EPO

Bladder Cancer

• Presents as painless hematuria + urinary symptoms + unilateral hydronephrosis
• Initial GOLD STANDARD is ⇒ Cystoscopy
• Followed by CT for staging
 

• Screening for bladder cancer in asymptomatic patients, including in patients who smoke or have a family history of bladder cancer, has not been shown to improve survival and is not recommended.

Renal Cysts

Characteristics of renal cysts	ㅤ
Simple renal cyst	Malignant cystic mass
Thin, smooth, regular wall	Thick, irregular wall
Unilocular	Multilocular
No septae	Multiple septae, occasionally thick & calcified
Homogeneous content	Heterogeneous content (solid & cystic)
Absence of contrast enhancement on CT/MRI	Presence of contrast enhancement on CT/MRI
Usually asymptomatic	May cause pain, hematuria, or hypertension
No follow-up needed	Requires follow-up imaging & urological evaluation for malignancy

 

Cysts

Benign:

Benign vs Malignant Cysts:

Vascular Disorders

Renal Vein Thrombosis

• Hypercoagulability

• Nephrotic Syndrome

• Malignancy

• Other (OCPs, Thrombophilia, Trauma, External Compression)

• Acute → Flank Pain + Hematuria (isolated) + High LDH (ischemia) + Increase kidney size on imaging (with NO hydronephrosis)

• Chronic → NO Renal symptoms

• CT or MR Angio OR Renal Venography

• Anticoagulation is usually enough

• If associated with AKI (usually caused by bilateral RVT) ⇒ Local Thrombolysis or Thrombectomy

Renal Artery Stenosis

• First Line ttt is ACEIs/ARBs
• MONITORING OF RENAL FUNCTIONS ARE MANDATORY DUE TO INCREASED IN CREATININE
• IF UNILATERAL RAS ⇒ other kidney compensates
• IF BILATERAL RAS ⇒ an increase of <30% allows for continuation
• If ALL MEDs FAIL/INTOLERANCE/RECURRENT FLASH PUL EDEMA/ REFRACTORY HF
• Renal Artery Stenting & Surgical Revascularization can be considered

Hypertensive Nephrosclerosis

• Characteristic Features:
• Elevated Creatinine (due to decreased GFR)
• US shows small atrophic kidneys bilaterally
• NO casts on urinalysis

Fibromuscular Dysplasia (FMD)

• Affects Renal & Internal carotid Arteries
• Abdominal Bruit
• Subauricular Bruit

• Dx → Imaging (Duplex US - CT/MRI Angio)

• TTT → ACEIs/ARBs for HTN
• Definitive management is PTA (Percutaneous Transluminal Angioplasty)
• If failed ⇒ Surgery

Hyposthenuria

• Definition → The inability of the kidneys to concentrate urine

• Common in patients with Sickle Cell Trait (patient has normal hct level & is asymptomatic) with family hx of SCD

• Increased tonicity in medulla causes sickling of RBCs in the vasa recta
• Resulting in inability of urine concentration ⇒ Polyuria despite adequate intake + diluted urine (low urine osmolality)
• Serum sodium is NORMAL as ADH is intact

• Treatment
• Mild in SCT → None
• SCD → RBC transfusion

Mixed Cryoglobulinemia Syndrome

• Chronic HCV infection causes B-cell activation & release of immunoglobulins that precipitate <37C (Cryoglobulins)
• Immunoglobulins (Polyclonal IgM & IgG with RF activity → binds to FC portion of IgG) & Hypocomplementemia

• Presentation: GN, PN, Palpable Purpura

Bladder & Urethral Disorders

Post-operative Urinary Retention

• Risk Factors:
• Patient Type: Increased age & male sex
• Surgery Type: Hernia repair, Arthroplasty, Anorectal operations, Abdominal & Pelvic Surgeries
• Anesthetic Factors:
• Prolonged anesthesia
• Use of meds (opioids, anticholinergics)
• hx of BPH
• hx of Neurological disease (dementia/cognitive impairmenet)

• Dx → Portable Bladder US
• Diagnosis is confirmed by ≥ 300ml urine
• if > 600 ml ⇒ Catheterization (???)

Posterior Urethral Valve

• Diagnosis:
• First Step ⇒ US
• If abnormal ⇒ Voiding Cystourethrogram

• Management:
• Bladder drainage & electrolyte correction
• Followed by Cystoscopy to confirm & ablate PUV

Urethral Stricture

• Males > Females

• Caused by hx of catheterization, Urethritis, Radiotherapy or commonly IDIOPATHIC (young man with no hx)

• Symptoms → Weak/Spraying Stream, Incomplete Emptying +/- irritative voiding

• Diagnosis:
• Suggested by elevated postvoid residual volume
• Confirmed by VCUG or Cystourethroscopy

• Management:
• Mild → Observe
• Severe → Urethral Dilation or Urethroplasty

Surgery

Pituitary Surgery Complications:

• Symptoms of Secondary Adrenal Insufficiency

• Post-op period can have symptoms of salt & water wasting from:
1. AVP-D (Central DI)
• Occurs during the first few days & usually resolves within a week
2. SIADH
• Occurs several days after the procedure & lasts for a few weeks

• So, post-op management includes:
• IMMEDIATE post-op evaluation for secondary adrenal insufficiency (measure morning cortisol → ACTH)
• Measuring of serum electrolytes for the first few days (to evaluate for both AVP-D & SIADH) & for several weeks after (to evaluate for SIADH)
 

Renal Injury

• Blunt Trauma + CVA tenderness + Flank pain +/- hematuria (gross or microscopic) ⇒ Renal Contusion
• FAST usually negative
• CT is done as bleeding is retroperitoneal

• Blunt Trauma + Flank pain/tenderness + Ecchymosis +/- Hematuria (gross or microscopic)
• Dx → CT Scan

Pediatrics

UTI in Children

• Risk Factors:
• Female
• Uncircumcised Male
• Urological abnormalities
• Bowel/Bladder Dysfunction (e.g. Constipation)

• Management:
• Antibiotics (for 1-2 weeks, preferably 3rd gen cephalosporins)
• Ciprofloxacin IS NOT used because it increases risk of cartilage damage
• CAN be used for pseudomonas infection in patients with indwelling catheters

The Following Investigations should be done AFTER the fever & symptoms have resolved:

• First Febrile UTI?
• Age < 2 years ⇒ Renal & Bladder US [Children <2 years are at a higher risk of complication, like HTN & renal scarring/damage, so renal anatomy should be assessed]
• If abnormal ⇒ Voiding Cystourethrogram
• Age ≥ 2 years ⇒ Observation alone
 
• Recurrent Febrile UTIs?
• Do ⇒ Renal & Bladder US
• If abnormal ⇒ Voiding Cystourethrogram
Indications of Voiding Cystourethrogram:
• ≥2 Febrile UTIs
• Abnormal Renal US
• Fever ≥ 39 with bacteria other than E.coli
• Signs of CKD (poor growth or HTN)

Hematuria in Children

 

Signs of UTI Infection:

• Dysuria

• Pyuria (WBCs in urine)

• Presence of nitrites OR leukocyte esterase in urine

 

If the cause was a UTI ⇒ Urinalysis should be repeated a few weeks after to ensure resolution of hematuria

• In contrast to non-hematuria UTI, clinical follow-up is sufficient

• If the patient doesn’t improve ⇒ Renal US is indicated to assess complications

 

Glomerular:

Low C3 → PSGN or SLE

• Diff via ASO & ANA

If all is negative → Kidney Biopsy indicated

Wilms Tumor

• Age: 2-5 years

• Presents as a large single heterogenous mass that doesn’t cross the midline that arises from WITHIN the superior pole of the kidney

• Other possible presentations:
• Varicocele that doesn’t reduce in supine position in a 4-year-old child (DO AUS)

• Management:
• First step ⇒ AUS (to differentiate it from other abdominal masses)
• THEN ⇒ MRI/CT (to evaluate extent of mass)
• Chest CT also done to check for pulmonary metastasis (most common site of mets)
Show Pic CT of Wilms tumor

Nocturnal Enuresis

• Greatest Risk Factor is Family Hx

• Desmopressin can be used for immediate ttt

• OSA (caused by tonsillar hypertrophy) [OSA in adults present as daytime solemnness, but for children it presents as behavioral concerns (ADHD like)]

• Encopresis (caused by fecal incontinence in presence of impacted stool) [ttt is laxative therapy which often resolves both constipation & enuresis]

• DM

Urinary Stasis due to chronic Constipation:

Vesicoureteral Reflux (VUR)

• Presents with a febrile UTI +/- hydronephrosis on US

Show Grades

• Voiding Cystourethrography confirms diagnosis & assesses severity/grade:
• SEVERE (reflux into ureter & kidney, causing structural damage) ⇒ Prophylactic abx +/- surgery
• MILD (causing NO structural damage) ⇒ Observation +/- prophylactic abx

Neonatal AKI

• Normal UOP in a neonate is ≥1 void per day

• If decreased = AKI
• Investigations:
• Hx of risk factors
• Volume status
• Renal & Bladder US
• THEN
• If hypovolemia ⇒ IV fluids

OBGYN

Proteinuria

• The Development of significant proteinuria [>300mg/day OR ≥1-2+ protein] PRIOR TO 20 WEEKS GESTATION ⇒ suggests and underlying kidney disease that was likely present BEFORE conception
• As a result DN + Pregnancy ⇒ Increases Creatinine
• NORMAL PREGNANCY ⇒ DECREASED creatinine

Ureteric Injuries

Urinary Incontinence

Stress Urinary Incontinence

• Management:
• FIRST LINE ⇒ Pelvic Floor (Kegel) Exercises +/- Pessary
• Miduretheral Sling Procedure

Urgency Urinary Incontinence

• Management:
• FIRST LINE ⇒ Pelvic Floor (Kegel) Exercises & Bladder Training
• IF fails → antimuscarinic therapy
• If not tolerable ⇒ Beta-3 Agonist (Mirabegron)

Urinary Tract Infections in Women

• Uncomplicated UTI (Urethritis/Cystitis)
• Preferred Empirical ttt is:
• TMP-SMX (for 3 days)
• Nitrofurantoin (for 5 days)
• Fosfomycin (single dose)
• FLUROQUINOLONES ARE USUALLY RESERVED FOR PATIENTS WHO CAN’T TAKE ABOVE MEDS ‘e.g. sulfa allergy’ / IN SETTINGS OF HIGH LOCAL RESISTANCE
📌
Urine Culture should also be performed in patients with uncomplicated cystitis who fail initial empirical abx therapy

• Complicated UTI (Pyelonephritis, Signs of systemic illness, pelvic pain in males)
• Outpatient (Stable) ⇒ Fluoroquinolones
• Inpatient (hemodynamically unstable) ⇒ ceftriaxone, piperacillin-tazobactam, carbapenems (eg, imipenem) WHILE AWAITING CULTURE RESULTS

Asymptomatic Bacteriuria in Pregnancy

• Def: ≥100,000 CFU/mL

• Most common CA: E.coli

• Complications: Acute Pyelonephritis & Preterm labor

• ttt:
• First Line is Fosfomycin & Beta-Lactams (Nitrofurantoin is avoided in 1st & 3rd trimesters)
• Repeat urine culture should be done due to risk for persistent or recurrent bacteriuria

Postpartum Urinary Retention

• Definition: inability to void ≥ 6 hours post vaginal delivery OR ≥6 hours post catheter removal following CS

• Risk Factors: Primi, Epidural anesthesia, pudendal nerve injury

• Causes Overflow Incontinence
• NEXT STEP ⇒ Urinary Catheterization
• Confirmed by ≥150mL
• Diagnostic & Therapeutic

Miscellaneous

Cyanide Toxicity

• Patient with hypertensive Emergency gets administered a Sodium Nitroprusside Drip
• Few hours later, he developed high-anion gap metabolic acidosis & Neurological Symptoms
• Caused by: Impairment of Mitochondrial Oxidative Phosphorylation

TMP

• Has a ENaC inhibition effect, causing potassium-sparing diuretic-like effect ⇒ Hyperkalemia & Increased Creatinine Levels (by inhibiting tubular creatinine secretion)
• Doesn’t actually change GFR

First-Gen Antihistamines

• Cause Urine Retention in elderly, especially those with BPH by inducing anti-cholinergic Side Effects on Detrusor Muscle

Calcific Uremic Arteriolopathy (Calciphylaxis)

• Systemic Arteriolar Calcification & Soft-tissue calcium deposition with local ischemia & necrosis

• Risk Factors: ESRD on hemodialysis, people who had renal transplantation

• Caused by high calcium, phosphate, PTH, and oral anticoagulants(warfarin)

Pics