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23 Cards in this Set
- Front
- Back
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Learning objectives
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Discriminate between common clinical presentations of coexistent hypertension and kidney disease and understand that these presentations represent different pathological lesions
Introduce the renal pathology and clinical presentation of a. arterionephrosclerosis b. malignant hypertension Discuss management of Hypertension in Chronic Kidney Disease Introduce new interventional technique for BP management: Renal Denervation |
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HTN stages
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Normal blood pressure: systolic <120 mmHg and diastolic <80 mmHg
Pre-hypertension: systolic 120-139 mmHg or diastolic 80-89 mmHg Hypertension: -Stage 1: SBP 140-159 mmHg or DBP 90-99 mmHg -Stage 2: SBP ≥160 or DBP ≥100 mmHg |
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Hypertensive nephrosclerosis: mechanisms, risk factors
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So called Benign hypertension
Mechanisms Multifactorial: -Increased sympathetic activity -Low renin salt sensitive or elevated renin -Genetic factors - family history Risk factors -Obesity -Alcohol (2 drinks/day) – 1.5 -2 fold increase -Race – 8-fold higher incidence of ESRD in African Americans -High salt intake – avg. intake of 100meq/day (2.3 g Na) -High fructose intake (>74g/day or 2.5 soft drinks/day) -Type A personality |
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Hypertensive nephrosclerosis (arterionephrosclerosis): pathology
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Often superimposed on other primary kidney diseases
Arteries and arterioles are involved On Gross examination: -Symmetrical small, atrophic kidneys in advanced stages -Diffuse fine granularity on the surface -Cortical scarring and shrinking of renal tissue |
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Arterionephrosclerosis: histology
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IMPORTANT
Vascular -Hypertrophic response to chronic hypertension manifested by MEDIAL HYPERTROPHY AND INTIMAL THICKENING leading to NARROWING OF VESSEL LUMEN -THICKENING OF WALLS of small arteries and arterioles -DEPOSITION of homogenous, pink HYALINE MATERIAL IN DAMAGED ARTERIOLAR WALL Renovascular disease may accelerate the development of secondary sclerotic lesion by enhancing ISCHEMIC NEPHRON LOSS Glomerular changes decrease blood flow → ischemia -Global or focal segmental sclerosis --Often attributed to ischemia resulting from arterial and arteriolar thickening --Possibly mediated by low birth weight, reduced nephron number, ApoL1 variants in African-Americans Interstitial nephritis – incompletely understood -Tubular atrophy with interstitial fibrosis -Ischemia induced immune response |
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Hypertensive emergency: definition, associations
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Hypertensive emergency:
-Acute -Life-threatening -Severe HTN ( > 180/120 mmHg) Associated with target organ damage -Retinal hemorrhages, exudates, papilledema -Renal (malignant nephrosclerosis) :acute renal failure, hematuria, proteinuria -Cerebrovascular: encephalopathy, atherothrombotic infarction, hemorrhage -Cardiac: dissection, LV failure, myocardial infarction -Acute pulmonary edema -Eclampsia Can occur with concomitant essential hypertension (untreated, undertreated, noncompliant), acute glomerulonephritis, renovascular hypertension, renal crises from collagen vascular disease |
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Accelerated malignant hypertension, hypertensive encephalopathy
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Clinical syndromes induced by severe hypertension
Accelerated Malignant Hypertension: -Severe HTN with papilledema, retinal hemorrhages or exudates - Renal: Malignant nephrosclerosis Hypertensive encephalopathy: -Severe headache and altered mental status -Signs of cerebral edema from hyperperfusion -Reversible with BP correction |
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Hypertensive urgency: definition
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Severe HTN
Often defined as SBP >180 and/or DBP >120 Asymptomatic No clinical evidence of end organ damage No proven benefit of rapid decrease BP |
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Mechanism of injury in malignant HTN
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Autoregulation failure
-Markedly elevated levels of plasma renin -Self perpetuating cycle --Increased Angiotensin II → intrarenal vasoconstriction → renal ischemia → increased renin secretion Rise in pressure in arterioles leads to disruption of vascular endothelium and increased permeability of small vessels to fibrinogen , other plasma proteins and fibrinoid material enters vessel walls FIBRINOID NECROSIS of arterioles Endothelial damage with platelet deposition Intravascular thrombosis Intimal smooth muscle hyperplasia |
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Malignant HTN: Treatment and prognosis
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True medical emergency
Prompt aggressive therapy – ICU care Avoid irreversible damage to target organs Prognosis -Overall survival has improved over time -Increased serum creatinine - 57% of pts. at 53 months -Pts. with renal failure have lower survival |
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Malignant HTN: morphology
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Normal sized kidney
“Flea-bitten” appearance due to pin point hemorrhagic spots Microscopy -FIBRINOID NECROSIS -Hyperplastic arterioles -Glomerular sclerosis |
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KDIGO recommendations CKD without diabetes
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If urine albumin excretion < 30 mg/24 hours
- ≤140 /≤90 If albumin excretion 30-300mg/24hours or > 300 mg/24 hours - ≤130/≤80 Recommend using ACEi or ARB in patients with > 30 mg/24 hours albuminuria IMPORTANT |
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KDIGO CKD and DM BP recommendations
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If albumin excretion < 30 mg/24hours
- ≤140/≤90 If albumin excretion > 30 mg/24 hours - ≤130/≤80 Use and ACEI or ARB if albumin excretion > 30 mg/24 hours IMPORTANT |
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KDIGO recommendations BP management in transplant
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≤130/≤80 irrespective of urinary albumin excretion (IF PT HAS A KIDNEY TRANSPLANT)
Consider time from transplantation, use of calcineurin inhibitors, presence or absence of albuminuria, comorbidities |
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KDIGO recommendations BP management children with CKD
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Start treatment with BP above 90th percentile for age, sex, height
Lower to 50th percentile Use ACEI or ARB irrespective of proteinuria |
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KDIGO recommendations for CKD and elderly
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Individualize therapy: no targets given
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Renal denervation: background
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Chronic elevation of the SNS is a key factor in hypertension, heart failure and chronic kidney disease
The renal sympathetic nerves are a major contributor to the complex pathophysiology of the elevated SNS activity and hypertension Therapeutic renal denervation (deliberate disruption of the nerves connecting the kidneys with the CNS ) is now possible and modulates the elevated SNS activity |
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Pathophysiology: baroreceptor control
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High pressure BARORECEPTORS of carotid sinus & aortic arch and low pressure of heart and great veins, activated by high BP or filling pressures send inhibitory signals to the nucleus tractus solitaris (NTS) and evoke reflex increases parasympathetic and decreased sympathetic activity RESULTING IN BRADYCARDIA AND PERIPHERAL VASODILATION
In primary hypertension, baroreceptors reset to defend higher BP |
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Excitatory neural reflexes
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Hypoxia activates carotid body CHEMORECEPTORS AND EVOKES REFLEX SYMPATHETIC STIMULATION
SENSORY AFFERENTS in the kidneys that project onto the NTS and evoke SYMPATHETIC Skeletal muscles innervated with sensory afferents that signal the brain of local mechanical and chemical changes during exercise to augment BP and increase muscle perfusion during exercise |
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Central sympathetic outflow
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Excitatory and inhibitory synaptic inputs from the NTS project centrally to neurons in the RVLM (rostral ventrolateral medulla), the site of sympathetic outflow from the brain
Preganglionic sympathetic fibers synapse in the adrenal medulla (to release EPI) and in the paravertebral sympathetic chain ganglia Postganglionic fibers, which release NE, innervate the heart, blood vessels and kidney |
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Effects of renal sympathetic nerve activity
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Increaseed renin secretion rate from juxtaglomerular cells
Increased renal tubular sodium reabsorption Renal vasoconstriction and decreased renal blood flow |
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Mechanism of BP control in renal denervation
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IMPORTANT
Reducing norepinephrine spillover Natriuresis Increasing renal blood flow Lowering plasma rennin activity Decreasing renal afferent signaling and central sympathetic activation |
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Future directions in HTN
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3 ongoing clinical trials regarding renal denervation in Europe
-For attenuation of CKD -RDN for native kidneys in patient with transplant for renoprotecion -Improving outcomes in cardiorenal syndrome |
