The Kidney and Hypertension Flashcards
Renal causes of HTN
Abnormalities in primary
Parenchymal dz
Vascular dz
Renal damage from HTN
Progression of chronic
Benign HTN nephrosclersis
Malignant nephroscleoriss
Salt sensitivie kidney
No matter how high the CO or TPR is, renal excretion has the capacity to return BP to normal
Therefore maintenance of crhonic HTN requires renal participation
Maybe result of decreased ability to excrete Na load…a higher AP required to maintan Na balance
Salt wasting disorders
Associated with low BP disorders
Salt sensitivity
High salt intake correlate with increase prevalene of ess HT
INceease sensitivity due to genetics…more in AA
OTher causes of salt-sensitive HTN
Low brith weight (nephron underdosing)
Primary glomerular dz
Aging, diabetes, obesity
Secondary HTN causes
Monogenetic tubular defects (Liddle syndrome)
Renal parenchymal
renal vascular dz
Renal parenchymal dz
Leading cause of HTN
RPomotes HTN and HTN promotes progression of kidney dz
Circle of HTN and kidney
Primary dz…dec neprhon number…hypertrophy and vasodilation of sruving neprhon and increased pressure…increase GFR and pressure…increase glomerular scelorisis…decrease neprhon number
COnstriction of the efferent arteriole and dilatio nof afferent to increase the pressure
Vascular causes of renal HTN
Ateromatous renal artery stenosis and fibromuscular renal artery hyperplasia
Renovascular HTN
Most commonly atherscelorsis
Less common fibromuscular dysplasia
Renovascular HTN clinical
Onset under 30 or over 55
SUdden onset uncontrolled in previously well controlled
Accelerated/malignant HTN
Intermittnet pulm edema
Epigastric bruit, particularly systolic/diastolic
Azotemia induced by ACEI
Unilateral small kdiney
Unexplained hypokalemia
Stensosi effects
INcreased renin…goes to AT2…Vasoconstriction, renal sodium retention, aldosterone secretion
Constricts efferent arteriole to help increase the GFR
Unilateral renal artery stenosis
Reduced perfusion…increased in RAAS system in that side…leads to increased renal perfusion in the ther kidney (increased Na excretion and suppressed RAS)
Effect of RAS blockade
Dx tests
Unilateral renal artery stenosis
Reduced AP, enhanced lateralization of diagnostic tests, GFR in stenotic kidney may fall
Plasma renin activity elevated
Lateralized features
ACEI effect in affected unilaterla renal steoniss dz
Will drop the GFR by dilating the effernt artieole
Bilateral renal stenosis path
Bilateral…reduced perfusion…activated RAS and impaired Na and water excretion…volume expansion so RAS is then turned off…then increased arterial pressure
Effect of blockade and dx tests of bilateral
Reduced arteril pressure only after volume depletion..may lower the GFR
Dx - plasma renin activity normal or low and no lateralized features
Renovascular HTN dx
Duplex doller US, CTA, MRA
Fibromuscular dysplasia
Young female 15-40
Medial in 90% and often in distal RA
Tx (PTRA) - successful in most…restenosis in 5-11, cured in 60
Total occlusion rare
Atheroscleotic RAS
Usually men over 55
ESRD in 11%
Progressesi n more than half
Tx is emphasis on medical managmenet…stent success is very high but cure is low
Medical rx of renovascular HTN
Aggressive risk fx mods
ACEI/ARB safe in unilateral if careful…but contraindiciated in bilateral RAS or solitary kidnye RAS
HTN nephrosclerosis
Due to HTN damage ot renal vasculature
Abnormalities in walls of small pre-glomeraular arterioles
Patchy ischemic atrophy gloemruli and less extent in the tubules
Slowly progressive renal failure
HTN neprhosclerosis demographics
Not everyone
Tx early on may help and less common than other HTN complications
Factors of developemnt of NTH neph
Degree of HTN
Transmission of pressure to glom
Tissue susceptibiltiy to barotrauama..pro-inflam or diabetes
Decreased neprhon mass
Pathh of HTN neprho
INcreased systemic pressure
Affarent constriction to dec intragolmerular pressure…efferent arteriole dilates
Hyaline arterioloscelrosis
Medial and intimal thickening
Mostly of the affarnet
Haline deposition caused by extravasation of proteins throgu hendothelium and partly by increase BM deposition
HYlainization of glmeruli
Narrowing of lumen of AA leads to dec blood flow and results in ischemia and glomerular damge
Hyalinization of glomerulus and loss of glomerular function
Tubular hyalizniation
Dec blood flow to the tubules and interstitium leads to cell death and loss of nephron function
Progressive loss of neprhons
Bad synergy with DM
Diabetic nephropathy increase in the RAA via AT2 leads to efferent arterial constriction further increased the glomerular HTN and accelerating the damage
Hx of patients with HTN nephro
HTN for a long time with evidence of uncontrolled BP
More comps than you think they should have
Features usggesting HTN neprho
Proteinuria is a big one
Black
HTN dx prior to proteinuria
LEft ventricular hypertrophy
HTN neprho tx
ACE inhibitors but diuretic needs ot be co-admin
HTN emergency
Severe HTN (diastolic above 120) with rapid decomp of organ system
OR life-therating conditions aggravated by presence of elevated BP
Lower over minutes ot horus
HTN emergency clinical cues
Moderate to severe HTN retinopathy (malignant HTN)
Severe asx HTN
Relatively asx or completely asx patient iwth a BP in the severe range…maybe a mild headache
Does NOT require rapid reduciton of BP
Rapid reduciton of BP may be harmful
BP reduced over a period of days
HTN emergencies clinical
Reflects consequens of BP on tagret organs
Depends on level and rate of BP
Affected by pre-existing HTN
CLinical pres of malignant HTN
HA - worse in morning Visual Ischemic CP Renal N//V Neurologic
Depends on involved organ system
Etiology of malignant
Essential HTN most common with renal parenchymal as seocndary
Pathophys of malignant
Crticial evaluiatioj of BP
Loss of autoregulation
Vascular endothelai damage - loss of permeability with deposition of fibrinogen and plasma proteins in walls…activation of mediators of coagulatio nand cell proliferation
Localized intravasc activation of clotting cascade - microangiopathic hemolytic anemia
Act of RAAS
Natriuresis from pressure
POsitive ffedback to increase more
Patho of Malig HTN
Proliferative endarteritis (onion skin)
Fibrinoid necrosis
Kidney - fibrinoid neprho of glomeruli, heorrhage and fibrosis of intersittium, tublar artophy or ATN
Microangiopathic hemolytic anemia
RBCs traverse an injured vascular endothelilum with associated fibrin depositon and platelet aggrgeation
Fragmentation hemolysis
Mech disruption of RBC membrane
IV hemolysis and appearance of schistocytes
Malignant HTN therpay
ICU
Arterial line
Rapid reduciton of MAP by 20%
160-170/100-110
SHort acting IV agents
Malig HTN prognosis
75% survive 5 years and 50% survive with restoration of pre-crisis renal function
