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Hypertension and Nephrology
The Salt story:
Homo-sapiens(humanrace) is 195000 yrs old, but salt has beenfreelyavailable to the humans
only since 150 yrs. It was difficultto obtain and was a highlyvalued trade item
Salts abilityto preserve foodbecame the foundationof civilization.
So we suddenlychangedform traditional lowsalt diet(50 to 100 mgs),which the kidneyshad
beenusedto since so millionsofyears, to a high salt diet(5 to 20 grams). Traditionally our kidneys
have beenprogrammedto conserve salt, not waste it. Thisis because,our kidneysare facing high
salt load only since last 200 years.And since these 200 years, there has beensuddenrise in the
percentage of hypertensives.
Salt appears to be BAD guy:
Increasedsaltintake hasbeenassociatedwith
1. increase inproteinuria
2. increasedcardiovascularmortality
3. leftventricularhypertrophy
4. resistance toantihypertensivedrugsandmanymore complications
Mechanismof the so called“Essential Hypertension”:
If an individual isgivenincreasedsaltintake overdays,there will be initialextracelluarfluid
volume expansion,transientincrease inhisbloodpressure.If he hasno tendencytodevelop
hypertension,thenhiskidneyswillexcreteall thatextrasaltthroughurine andhe will have normal
extracellularvolumeandhisbloodpressure will returntonormal.
If his kidneysdonothave the abilitytoexcrete all thatextrasaltthroughhisurine,thenhe will
develophypertension.The kidneysabilitytoexcretesaltdependsongeneticvariationsof the various
Sodiumchannelspresentinthe tubulesof the kidneys.
So if someone ishypertensive (essential,withpositivefamilyhistory),itjustmeansthathis
kidneysdonothave the abilitytoexcrete the necessaryextrasalt.
Classification of HT (JNC- 7)
Classification SystolicBP Diastolic BP
Normal below120 below 80
Prehypertension 120–139 80–89
Stage 1 HT 140–159 90–99
Stage 2 HT 160+ 100+
.
Thisnewconceptof pre- hypertensionhasbeenadded.Itindicatespeople whowill develop
hypertensioninlaterlife (highrisk).Thisprehypertensionneedstobe treatedinspecificsiturationslike:
diabetics,coronaryarterydisease andchronickidney disease.
Secondary hypertension
• Severe orresistanthypertension
• An acute rise inbloodpressure overapreviouslystablevalue
• Provenage of onsetbefore puberty
• Age lessthan30 yearswithno familyhistoryof hypertensionandnoobesity
Causesof secondaryHypertension:
• Renal:
– Renal parenchymal disease
– Reno– vasculardisease:
• Drugs:
– NSAIDS:brufen,Inac,nimusulides
– Corticosteroids
– Oral contraceptive pills
– Certainanti-depressantmedications
Endocrine causes:
– Cushingssyndrome
– Hypothyroid andhyperthyroidism
– Pheochromocytoma
• Triad of headache (usuallypounding),palpitations,andsweating
Sleepapneasyndrome
Coarctationof aorta
Whom to treat:
Pre-hypertension:
life style modificationinall:diet,exercise,stopsmoking,weightreduction,moderatealcohol,salt
restriction
Hypertension:
Choice of agents:
• Thiazide-type diuretics
• Angiotensinconvertingenzyme inhibitorsandangiotensinIIreceptorblockers
• Calciumchannel blockers
• Beta blockers,whichare nowusedlessoftenfor initial therapyinthe absence of aspecific
indicationfortheiruse
Monotherapy:
• lowdose thiazide diuretic- hydrochlorthiazideandchlorthalidone
• Angiotensinconvertingenzyme (ACE):ramipril,enalapril
• InhibitorangiotensinIIreceptorblocker(ARBs):Telmisartan,Losartanandolmesartan
• long-actingdihydropyridine calciumchannel blocker- amlodepineandNifedepineretard.
Combinationtherapy
• ACEIinhibitorplusamlodepine
• ARB plusAmlodepine
• ACEI/ARB plushydrochlorthiazide
• Triple combination:abetablockerlike atenololormetoprolol istobe added
• Furthermore additionsinsevere HT:
– Moxonidine orclonidine (Arkamin)
– Prazocin- alphablocker
– Alphamethyldopa- pregnancy
– Minoxidil-directvasodialtor
– Seldenephil –NOstimulation(directvasodilator)
– Labetelol
– hydrallazine
Cautions with drugs:
• Thiazides:
– Impairedlipidprofile
– Hypokalemiaand severe hyponatremia(elderly)
– Hypovolemia
• Beta blockers:
– impairedglucose tolerance andincreasedriskof new onsetdiabetes
– Bradycardia
– Worseningof COPD
– Higherriskof stroke inelderly
• ACEIand ARBs
– Worseningof renal function
– Hyperkalemia
– Cough
– Monitoringnecessary
– Cautionduringpregnancy
• Calciumchannel blockers:
– Safe drugs
– Edemaoverfeet
– Palpitations
headache

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Hypertension and nephrology

  • 1. Hypertension and Nephrology The Salt story: Homo-sapiens(humanrace) is 195000 yrs old, but salt has beenfreelyavailable to the humans only since 150 yrs. It was difficultto obtain and was a highlyvalued trade item Salts abilityto preserve foodbecame the foundationof civilization. So we suddenlychangedform traditional lowsalt diet(50 to 100 mgs),which the kidneyshad beenusedto since so millionsofyears, to a high salt diet(5 to 20 grams). Traditionally our kidneys have beenprogrammedto conserve salt, not waste it. Thisis because,our kidneysare facing high salt load only since last 200 years.And since these 200 years, there has beensuddenrise in the percentage of hypertensives. Salt appears to be BAD guy: Increasedsaltintake hasbeenassociatedwith 1. increase inproteinuria 2. increasedcardiovascularmortality 3. leftventricularhypertrophy 4. resistance toantihypertensivedrugsandmanymore complications Mechanismof the so called“Essential Hypertension”:
  • 2. If an individual isgivenincreasedsaltintake overdays,there will be initialextracelluarfluid volume expansion,transientincrease inhisbloodpressure.If he hasno tendencytodevelop hypertension,thenhiskidneyswillexcreteall thatextrasaltthroughurine andhe will have normal extracellularvolumeandhisbloodpressure will returntonormal. If his kidneysdonothave the abilitytoexcrete all thatextrasaltthroughhisurine,thenhe will develophypertension.The kidneysabilitytoexcretesaltdependsongeneticvariationsof the various Sodiumchannelspresentinthe tubulesof the kidneys. So if someone ishypertensive (essential,withpositivefamilyhistory),itjustmeansthathis kidneysdonothave the abilitytoexcrete the necessaryextrasalt. Classification of HT (JNC- 7) Classification SystolicBP Diastolic BP Normal below120 below 80 Prehypertension 120–139 80–89 Stage 1 HT 140–159 90–99 Stage 2 HT 160+ 100+ . Thisnewconceptof pre- hypertensionhasbeenadded.Itindicatespeople whowill develop hypertensioninlaterlife (highrisk).Thisprehypertensionneedstobe treatedinspecificsiturationslike: diabetics,coronaryarterydisease andchronickidney disease.
  • 3. Secondary hypertension • Severe orresistanthypertension • An acute rise inbloodpressure overapreviouslystablevalue • Provenage of onsetbefore puberty • Age lessthan30 yearswithno familyhistoryof hypertensionandnoobesity Causesof secondaryHypertension: • Renal: – Renal parenchymal disease – Reno– vasculardisease: • Drugs: – NSAIDS:brufen,Inac,nimusulides – Corticosteroids – Oral contraceptive pills – Certainanti-depressantmedications Endocrine causes: – Cushingssyndrome – Hypothyroid andhyperthyroidism – Pheochromocytoma • Triad of headache (usuallypounding),palpitations,andsweating Sleepapneasyndrome Coarctationof aorta Whom to treat: Pre-hypertension:
  • 4. life style modificationinall:diet,exercise,stopsmoking,weightreduction,moderatealcohol,salt restriction Hypertension: Choice of agents: • Thiazide-type diuretics • Angiotensinconvertingenzyme inhibitorsandangiotensinIIreceptorblockers • Calciumchannel blockers • Beta blockers,whichare nowusedlessoftenfor initial therapyinthe absence of aspecific indicationfortheiruse Monotherapy: • lowdose thiazide diuretic- hydrochlorthiazideandchlorthalidone • Angiotensinconvertingenzyme (ACE):ramipril,enalapril • InhibitorangiotensinIIreceptorblocker(ARBs):Telmisartan,Losartanandolmesartan • long-actingdihydropyridine calciumchannel blocker- amlodepineandNifedepineretard. Combinationtherapy • ACEIinhibitorplusamlodepine • ARB plusAmlodepine • ACEI/ARB plushydrochlorthiazide • Triple combination:abetablockerlike atenololormetoprolol istobe added • Furthermore additionsinsevere HT: – Moxonidine orclonidine (Arkamin) – Prazocin- alphablocker – Alphamethyldopa- pregnancy – Minoxidil-directvasodialtor – Seldenephil –NOstimulation(directvasodilator) – Labetelol – hydrallazine
  • 5. Cautions with drugs: • Thiazides: – Impairedlipidprofile – Hypokalemiaand severe hyponatremia(elderly) – Hypovolemia • Beta blockers: – impairedglucose tolerance andincreasedriskof new onsetdiabetes – Bradycardia – Worseningof COPD – Higherriskof stroke inelderly • ACEIand ARBs – Worseningof renal function – Hyperkalemia – Cough – Monitoringnecessary – Cautionduringpregnancy • Calciumchannel blockers: – Safe drugs – Edemaoverfeet – Palpitations headache