NP18 Nephrology

Parenchymal Kidney Diseases

Essential Med Notes 2015

Risk Factors
>50 yr old
smoking
other atherosclerotic disease (dyslipidemia, DM, diffuse atherosclerosis)
Signs and Symptoms
severe/refractory HTN and/or hypertensive crises, with negative family history of HTN
asymmetric renal size
epigastric or flank bruits
spontaneous hypokalemia (renin activation in under-perfused kidney)
increasing Cr with ACEI/ARB
flash pulmonary edema with normal LV function
Investigations
must establish presence of renal artery stenosis and prove it is responsible for renal dysfunction
duplex Doppler U/S (kidney size, blood flow): good screening test (operator dependent)
digital subtraction angiography (risk of contrast nephropathy)
CT or MR angiography (effective noninvasive tests to establish presence of stenosis, for MR
avoid gadolinium contrast if eGFR <30 mL/min because of risk of systemic dermal fibrosis)
ACEI renography (e.g. captopril renal scan)
renal arteriography (gold standard)
Treatment
surgical: percutaneous angioplasty stent, surgical revascularization, occasionally surgical
bypass
medical: BP lowering medications (ACEI is drug of choice if unilateral renal artery disease but
contraindicated if bilateral renal artery disease)
little or no benefit if therapy is late (e.g. kidney is already shrunken), however, therapy can be
considered to save the opposite kidney if normal
3. RENAL VEIN THROMBOSIS
Etiology
hypercoagulable states (e.g. nephrotic syndrome, especially membranous), ECF volume
depletion, extrinsic compression of renal vein, significant trauma, malignancy (e.g. RCC),
sickle cell disease
clinical presentation determined by rapidity of occlusion and formation of collateral circulation
Signs and Symptoms
acute: N/V, flank pain, hematuria, elevated plasma LDH, rise in Cr, sudden rise in proteinuria
chronic: PE (typical first presenting symptom), increasing proteinuria and/or tubule dysfunction
Investigations
renal venography (gold standard), CT or MR angiography, duplex Doppler U/S
Treatment
thrombolytic therapy percutaneous thrombectomy for acute renal vein thrombosis
anticoagulation with heparin then warfarin (1 yr or indefinitely, depending on risk factors)
SMALL VESSLE DISEASE
1. HYPERTENSIVE NEPHROSCLEROSIS
see Hypertension, NP31
2. ATHEROEMBOLIC RENAL DISEASE
progressive renal insufficiency due to embolic obstruction of small- and medium-sized renal
vessels by atheromatous emboli
spontaneous or after renal artery manipulation (surgery, angiography, percutaneous angioplasty)
anticoagulants and thrombolytics interfere with ulcerated plaque healing and can worsen
disease
investigations
eosinophilia, eosinophiluria, and hypocomplementia
renal biopsy: needle-shaped cholesterol clefts (due to tissue-processing artifacts) with
surrounding tissue reaction in small-/medium-sized vessels
treatment
no effective treatment; avoid angiographic and surgical procedures in patients with diffuse
atherosclerosis, medical therapy for concomitant cardiovascular disease
prognosis: poor overall, at least a third will develop ESRD

Stenting and Medical Therapy for

Atherosclerotic Renal Artery Stenosis
NEJM 2014;370:13-22
Study: Multicenter, unblinded RCT, median followup of 43 mo.
Patients: 947 patients with atherosclerotic renalartery stenosis who also have significant systolic
HTN or CKD.
Intervention: Percutaneous revascularization
(stenting) with medical therapy (statins, ARB,
calcium channel blockers, HCTZ and BP control) vs.
medical therapy alone.
Outcomes: Occurrence of adverse CV or renal
event (composite of death from CV or renal cause,
MI, stroke, hospitalization for CHF, progressive
renal insufficiency, or need for renal replacement
therapy) and all-cause mortality.
Results: No significant difference in primary
composite end point between participants who
received stenting or those on medical therapy
alone. No significant differences between the
treatment groups in the rates of the individual
components of the primary end point or in all-cause
mortality.
Conclusion: Renal artery stenting did not confer a
significant benefit with respect to the prevention
of clinical events when added to comprehensive,
multifactorial medical therapy in people with
atherosclerotic renal artery stenosis and HTN
or CKD.