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Renal Function and Failure

Nephron basics

• Proximal convoluted tubule: reabsorbs 65% Na, K, Ca, 80% Phos, H₂O, bicarb, and 100% glucose and amino acids, also generates ammonia from glutamine (urinary acidification)
• Loop of Henle: absorbs 25-30% Na and concentrates the interstitium, descending limb water permeable, ascending limb water impermeable
• Distal convoluted tubule: absorbs Na, Ca
• Collecting tubule: absorb Na via principal cells, H via intercalated cells, K by both

Sodium balance

• Regulated by ADH (free water)
• Assess fluid status: skin turgor, blood pressure
• Sodium repletion: 3% saline at 1mL/kg/hr, do not exceed 8-12mmol/L/d (can cause cerebral demyelination)

Potassium balance

• Hypokalemia: seen with GI loss, renal loss, systemic alkalosis, medications, postobstructive diuresis, and hyperaldosteronism
• Hyperkalemia: seen with impaired renal excretion, systemic acidosis
• Bicarbonate, insulin + glucose, and albuterol used to drive K intracellularly, does not cause K losses
• K excretion: induce with kayexalate or lokelma (K-binding exchange resin), diuretics, and hemodialysis
• Calcium gluconate: prevents cardiac complications (stabilizes myocytes) when EKG changes seen

Acid/Base balance

• Concentration alkalosis: volume depletion causes Na retention, bicarb absorption, and net loss of H
• Respiratory acidosis: elevated CO₂ leads to increased renal H secretion
• Renal failure: decreased bicarb filtration leads to increased H loss
• Hyperaldosteronism: increased Na absorption causes increased H losses

Renal Tubule Acidoses

• Type I: unable to secrete H in distal nephron, causes hyperchloremic metabolic acidosis, urine pH > 5.5, low serum bicarb, low urine citrate, CaPhos stones
• Type II: unable to absorb bicarb in proximal tubule
• Type IV: decreased H and K secretion in collecting duct

Kidney Injury

Acute kidney injury causes

• Prerenal AKI: caused by renal hypoperfusion, decreased FENa, reversible after removing underlying cause and improving renal perfusion
• Intrarenal AKI: caused by glomerular/tubular injury, requires diagnosis and treatment of specific cause
• Postrenal AKI: caused by urinary tract obstruction, can result in postobstructive diuresis after resolution with resultant water/salt wasting
• Acute interstitial nephritis (AIN): rash 15%, fever 27%, eosinophilia 23%, diagnose with high suspicion, WBC casts, and renal biopsy
• Renal vein thrombosis: seen with nephrotic syndrome and malignancy, presents with flank pain + hematuria + elevated LDH + swollen kidney on imaging
• Assessing AKI: volume status, cardiac history, liver/renal failure, DM, recent surgery, medications, contrast, bleeding, serum/urine electrolytes
• Fractional Excretion of Na (FENa): (UNa * SCr) / (SNa * UCr), cutoff 1%
• Fractional Excretion of Urea (FEUrea): (Urea * SCr) / (SBUN * UCr), cutoff 35%

Management of intrarenal AKI

• Contrast nephropathy: unclear if a true diagnosis, prevent with IV hydration
• Rhabdomyolysis: IV hydration + bicarbonate (monitor in ICU)
• Tumo caused by uric acid crystal precipitation and hyperphosphatemia, can consider prophylactic rasburicase (converts uric acid to allantoin)
• Can give loop diuretics, good response indicates favorable prognosis, diuretic use does not worsen or improve AKI recovery

Renovascular Hypertension

Renal artery stenosis

• Narrowing of renal artery > 50% normal luminal diameter
• Most common cause of renovascular HTN
• 60-80% are atherosclerotic, the remainder are fibromuscular dysplasia
• Causes 5-15% total renal failure in ages > 50
• Duplex ultrasonography is best screening test, although arteriography is gold standard, can use CT/MR

Criteria for workup of renovascular HTN

• Severe/refractory HTN with Grade III-IV hypertensive retinopathy
• Sudden onset moderate/severe HTN in previously normotensive or well-controlled hypertensive
• HTN before 20yo or after 50yo
• Unexplained worsening renal function with(out) HTN or after starting ACEi/ARB or with improved BP with other antiHTN medications
• Worsening HTN with diuretics
• Unexplained recurrent heart failure episodes
• Abdominal bruit that radiates bilaterally
• Diffuse vascular disease and/or cholesterol emboli

RAS Management

• Unilateral stenosis: induces HTN due to normal kidney excreting water/salt and vasoconstriction from angiotensin, resolves with treatment of stenosis, ACEi/ARB
• Bilateral stenosis: induces HTN due to inability to excrete water/salt and subsequent volume expansion, resolves with treatment of stenosis
• AntiHTN meds can cause renal ischemia distal to obstruction, monitor renal function
• Percutaneous transluminal renal artery angioplasty (PTRA): dilation with balloon, optimal lesions are < 1cm, partially occluded, and not involving ostium, restenosis rates 15-25%
• Stenting: unclear benefit, still require medical therapy
• Surgery: indicated for aneurysmal/occlusive aortic disease, macroaneurysms, or rapidly worsening HTN/renal function
• Monitoring: screen with doppler US and labs to assess for changes in renal function

Fibromuscular dysplasia types

Type	% total	Cause	Demographic	Location	Angiographic appearance	Progression?	Renal Failure?
Medial fibroplasia	75-85%	Medial layer fibrosis	Women 25-50yo	Distal renal artery extending into branches	String of beads	Minimal	No
Perimedial fibroplasia	10-25%	Collagen deposits in outer medial layer	Women 5-15yo	Midrenal artery extending into branches	String of beads	Yes (occlusion)	Yes
Intimal fibroplasia	10%	Collagen deposits in intimal layer	Children and young adults	Proximal renal artery	Stenosis with distal aneurysm/dissection	Yes (occlusion)	Yes
Medial hyperplasia	2-3%	Smooth muscle hyperplasia without fibrosis

FMD management

• Continue medical management if long-standing HTN
• Perform PTRA for young/healthy patients prior to HTN onset, or for patients with poorly controlled HTN
• All patients with FMD should take ASA 81
• Surveill with labs, BP checks, and doppler US to assess for worsening or recurrence

Renal artery aneurysms

• Usually asymptomatic (incidentally diagnosed on CT/XR), may present with flank pain, hematuria, or HTN
• Asymptomatic repair criteria: ≥ 2cm, uncontrolled/resistant HTN, potential future pregnancy
• Symptomatic repair criteria: perinephric/retroperitoneal bleeding, renal ischemia/infarction, gross hematuria
• Management: open repair, robotic repair, endovascular stenting/occlusion

Renal Transplant

Who gets a transplant?

• Indications: ESRD, CKD 5, and CKD 4 with GFR ≤ 20
• Absolute contraindications: severe/advanced vascular or pulmonary disease, active/untreated infections, intermediate/high stage malignancy in past 3 years, major psychiatric illness
• Relative contraindications: life expectancy < 5yrs independent of renal disease, medical nonadherence, substance use, BMI > 40, poor functional status

Workup to ensure good transplant candidacy

• History: cause of ESRD, hx ESRD management, comorbidities
• Exam: assess for vascular disease, abdominopelvic surgical scars
• Lab: CBC, CMP, coags, UA, urine P/C ratio, HCG, infectious workup (CMV, EBV, VZV, HBV, HCV, HIV, syphilis, TB)
• Tissue matching: assess ABO, HLA
• Imaging: abdominopelvic CT/US to assess for disease, anastomotic sites, and surgical complicating factors
• Cardiac workup: EKG, CXR, consider stress test if multiple cardiovascular risk factors
• Malignancy eval: screen per guidelines, wait 1yr after treatment of localized or low stage disease, 5yrs for intermediate/high stage disease
• Donor eval: history, physical, lab/infectious workup, renal assessment (left kidney preferred for donation due to vessel length)

Urologic "clearance" for transplant

• LUTS: does not need to be worked up or treated prior to transplant unless underlying cause of ESRD (BPH/VUR/NGB), recurrent UTIs, or prior interventions
• Interventions may result in scar tissue (stricture/BNC) in patients with minimal urine output
• Delay BPH interventions 1-2mo after transplant to decrease infectious complications
• Stones: do not need to treat if asymptomatic, treat if causing infections
• Decreased bladder capacity: usually improves post-transplant, does not require workup or augmentation

Complications

• Acute hematuria: usually resolves within days and rarely requires irrigation, usually from anastomosis
• Post-biopsy hematuria: can be development of fistula, 70% spontaneously resolve, otherwise can embolize
• Other hematuria: follow normal hematuria workup, consider cytology and urine BK titers
• Retained stent: 0-6%, encrustation does not cause symptoms due to lack of innervation
• Urine leak: 1-9%, usually due to distal ureteral ischemia, follow drain and urine output, drain will have elevated creatinine, place foley + PCN, may improve with diversion alone (36-87%) but stenosis may develop and require individualized repair
• Ureteral stricture: 1-9%, usually due to distal ureteral ischemia, consider when renal failure and hydronephrosis occur, hydronephrosis may be less than expected due to perirenal fibrosis, provide drainage and assess for obstruction, repair endoscopically or with open/lap technique
• Vesicoureteral reflux: 50-86%, symptomatic in < 1%, may increase HTN/sepsis risk, confirm with VCUG, improve voiding pressures, can consider deflux vs reimplant
• Lymphocele: 0.6-33%, symptomatic in 0.03-26%, usually diagnosed within 6mo, confirm with imaging and drainage, most resolve spontaneously (< 15% will require treatment), can aspirate +/- sclerotherapy, drainage, decortication/marsupialization
• Infections: treat for 7-10 days if transplanted within 6mo, otherwise 5-7 days, 14-21 days for pyelonephritis/sepsis, treatment of asymptomatic bacteruria not recommended
• Kidney stones: 1%, can observe nonobstructing stones < 4mm, otherwise treat per stone algorithms
• LUTS: may be undiagnosed due to oliguria/anuria, normal voiding should improve with bladder filling, preoperative management of small bladder not required, delay TURP until 3 weeks post-transplant (high risk for sepsis/death)
• Kidney cancer: manage both native and transplant kidneys per guidelines (do not partial nephrectomize native kidneys), no benefit in screening unless preexisting risk factors
• Bladder cancer: 3x increased risk, can use BCG even if immunocompromised, otherwise manage per guidelines
• Prostate cancer: no need to screen as part of pretransplant workup, active surveillance underutilized