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153 Cards in this Set
- Front
- Back
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Tubuloglomerular feedback (2)
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Volume overload -> fast flow rate, lots of Na, Cl not reabsorbed -> high concentration at macula densa -> afferent arteriole constriction
Volume depletion -> slow flow rate -> lots of Na, Cl reabsorption so little in filtrate -> RAA -> preferential efferent vasoconstriction |
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Mechanisms of Na reabsorption (4)
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PT - Na/H exchangers + Na cotransporters (amino acids . .) 67%
LOH - Na/K/Cl cotransporter 25% DT - Na/Cl cotransport 4% CT - Na+ channels 3% |
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GFR equation
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GFR = Lp * S (Pgc - Pbs - pi_gc)
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How is filtration fraction adjusted at hypo or hypertension
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Hypertension - high RPF -> afferent arteriolar vasoconstriction lowers Pgc
Hypotension - low RPF -> efferent arteriolar constriction increases Pgc |
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What do prostaglandins do in volume depletion?
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Dilate afferent arteriole
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Clearance equation
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Cx = UxV / Px
U = urine concentration V = urine flow rate P = plasma concentration (Ux*V = amount of x excreted in urine) |
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5 conditions that increase GFR
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Mesangial cell relaxation
Afferent arteriole dilation (PGE) Efferent arteriole constriciton (AII) Hypoalbuminemia High RPF (oncotic pressure rises slower during ultrafiltration) |
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5 conditions that decrease GFR
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Mesangial cell contraction AII
Afferent arteriole constricition (NSAIDs) Efferent arteriole dilation (ACEi, ARB) Hypotension or volume depletion Increased tubular pressure (urinary obstruction) |
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How much Na and H2O are typically reabsorbed?
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99%
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Bartter Syndrome
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Deficit in Na/K/Cl cotransporter in LOH
Think loop diuretics |
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Gitelman Syndrome
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Defective Na/Cl cotransporter in distal tubule
Think thiazide diuretics |
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Liddle Sydrome
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Constitutively activated Na+ channel in collecting tubule lead to volume overload and excessive Na retention and hypokalemia (excessive K excretion due to overactive Na+ leaving a negative charge in lumen)
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Urine osmolality in relation to ADH
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ADH present - aquaporins lead to H2O reabsorption and maximally concentrated urine (1200)
ADH absent - maximally dilute urine (40) |
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How is Na reabsorption related to bicarb in the proximal tubule? (4)
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1. Na is reabsorbed in exchange for secretion of H+
2. Luminal H+ + HCO3- -> H2CO3 -> H2O and CO2 by carbonic anhydrase 3. CO2 goes into cell and is converted back to HCO3- 4. Cytoplasmic HCO3- crosses basolateral membrane via HCO3-/Cl- antiporter or Na/HCO3- symporter |
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What do carbonic anhydrase inhibitors do?
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Block luminal conversion of H+ to HCO3- and thus block H+ exchange for Na+
Act as diuretics |
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Sodium balance sensors (3)
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Volume not Na content!
Afferent arteriole Atria Carotid sinus |
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Sodium balance effectors (4)
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RAA
ANP NE ADH |
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Sodium balance: what is affected?
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Tubular Na handling
Thirst |
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What is the main indicator of water balance?
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Plasma osmolality (Na concentration)
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Water handling (sensors, effectors, what is affected)
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Sensors: hypothalalmic osmoreceptors
Effectors: ADH, thirst What is effected: urine osmolality, water intake |
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When is PTH released?
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Low calcium
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What does PTH do? (3)
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Mobilize Ca from bone
Stimulate Ca reabsorption from distal tubule Lead to 1, 25-hydroxylation of vitamin D in kidney -> stimulates Ca absorption from gut |
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Volume sensors (4)
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Macula densa
Afferent arteriole Cardiac chambers Carotid bodies |
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How does HF cause volume overload?
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heart fails -> low ECV -> Na retention -> volume overload
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How does cirrhosis cause volume overload? (2 ways)
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impaired albumin synth -> decreased plasma oncotic pressure -> decreased Pgc -> Na retention/volume overload
OR Arteriovenous malformation -> decreased SVR and bp -> renal underperfusion -> Na retention/volume overload |
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How does nephrotic syndrome cause volume overload?
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Protein loss in urine -> decreased plasma oncotic pressure -> decreased Pgc -> Na retention/volume overload
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Cardiac chamber response to volume overload
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Increased stretch -> ANP release -> blocks Na+ channels in CT
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Factors stimulating renin release from juxtaglomerular apparatus (3)
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Decreased Na/Cl at macula densa
Decreased afferent arteriole pressure B1 sympathetic stimulation of JGA |
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Actions of angiotensin II (4)
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Systemic vasoconstriction
Efferent arteriole > afferent vasoconstriction Na reabsorption in PT Aldosterone release -> Na+ reabsorption in CT |
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Factors stimulating aldosterone synthesis (2)
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Angiotensin II
Hyperkalemia |
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Actions of aldosterone at CT (3)
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Enhanced Na reabsorption
Enhanced K secretion Enhanced H secretion |
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Actions of aldosterone at CT (3)
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Enhanced Na reabsorption
Enhanced K secretion Enhanced H secretion |
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Factors stimulating SNS
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Decreased pressure at carotid and aortic bodies
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Actions of sympathetic nervous system in response to low volume (4)
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Sympathetic vasoconstriction
Efferent arteriole vasocontriction Renal Na retention at PT Renin release |
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FENa (definition and meaning in AKI)
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excreted sodium / filtered sodium
In AKI, if FENa is < 1, means tubular cells are responding normally to Na levels |
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Cirrhosis and volume overload: overfill vs underfill
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Overfill: AV malformation -> decreased SVR -> low ECV -> Na retention/volume overload -> ascites
Underfill: ascites first -> volume depletion -> Na retention |
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Appropriate vs inappropriate ADH
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Appropriate - ADH release is triggered by carotid barorecpetors due to ineffective circulating volume -> hypoosmolality
Inappropriate - no discernible trigger for ADH release - hypothyroidism, SIADH |
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Hypo-osmolality Rx (2)
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Suppress or block (vaptans) ADH
Don't raise serum Na by more than .5 meq/L |
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Diabetes insipidus
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Impaired ADH production (neurogenic) or impaired ADH response (nephrogenic)
Dilute urine in the setting of hyperosmolality |
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Fatty casts
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Nephrotic syndrome
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Muddy brown casts
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ATN
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WBC casts
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Allergic interstitial nephritis
or pyelonephritis |
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RBC casts
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Glomerulonephritis
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K+ reabsorption and secretion
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67% in PT paracellularly
20% in LOH via Na/K/Cl cotransport Regulated secretion in CT by aldosterone |
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Where do K-wasting diuretics block Na reabsorption?
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LOH and DT
Cause lots of Na to be in CT, stimulates K+ secretion as well as activate RAA and aldosterone |
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Where do K-sparing diurects act?
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CT
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What makes K+ move intracellularly? (3)
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Alkalemia
Insulin Catecholamines |
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What makes K+ move extracellularly? (4)
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Acidemia
Glucagon Exercise Hyperosmolality (via solvent drag) |
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Hypokalemia clinical (3)
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Weakness
Paralysis Arrythmia |
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Hyperkalemia treatment (3)
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Stabilize cardiac membrane with Ca
Move K into cells (insulin, catecholamines, HCO3) Increase K excretion (K-wasters, resin binders) |
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Henderson equation
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[H+] = PaCO2 / [HCO3-]
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What happens to the daily endogenous acid load?
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50% is buffered by extracellular bicarbonate
Remainder is buffered by extra- and intra-cellular and bone buffers |
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Two main functions of renal acid excretion
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Reclamation of filtered bicarb
Net acid excretion |
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Simple respiratory acidosis (3)
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Hypercapnia
Acidemia Secondary bicarb increase |
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Chronic adaptation to respiratory acidosis (2)
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Increase in ammonia genesis for H+ excretion - transient
Increase in renal bicarb reabsorption - persistent |
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Simple respiratory alkalosis (3)
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Hypocapnia
Alkalemia Secondary bicarb decrease |
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Chronic adaption in respiratory alkalosis
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Transient decrease in urinary net acid excretion (primarily via less NH3 excretion
Persistent decrease in bicarb reabsorption |
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Mineral vs organic acid loads
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Mineral - non AG
Organic - AG |
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Acidosis in CKD (types and progression)
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Decreased ammoniagenesis -> decreased H+ excretion -> Non-AG metabolic acidosis
As CKD progresses normally excreted organic acids are retained -> AG metabolic acidosis |
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Distal renal tubular acidosis (anion gap?)
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Impaired H+/ATPase secretion in CT
Non-AG acidosis |
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Proximal renal tubular acidosis
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Carbonic anhydrase inhibitor prevents HCO3 absorption and H+ excretion
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Anion gap equation
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Na - Cl - HCO3-
normally 12 > 12 defines an organic metabolic acidosis |
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Non-anion gap acidosis (2 most common and treatment)
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Diarrhea (bicarb loss)
CKD Treat w/ bicarb replacement |
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Lactic acidosis (cause and rx)
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Anion gap
Inadequate perfusion -> pyruvate to lactate Rx - restore perfusion to allow liver to convert lactate to bicarb |
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Ketoacidosis (cause, sign, and rx)
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Insulin deficiency -> altered hepatic metabolism to ketoacid production
Also have hyperglycemia -> hyperosmolality -> hyperkalemia w/ total body K depletion and massive H2O and electrolyte loss Rx - insulin, electrolyte and H2O replenishment |
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Major causes of metabolic acidosis (3 broad categories)
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Bicarb loss (diarrhea, prox RTA)
Increased acid load (organic vs mineral) Impaired acid excretion (CKD, distal RTA) |
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Clinical manifestations of metabolic acidosis (3 broad)
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Respiratory - incr alveolar ventilation w/ decreased PaCO2
Cardio - arrhythmia, impaired response to catecholamines GI - nausea/vomiting, ab pain, diarrhea |
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What is the main difference b/w Cl responsive and resistance alkalosis?
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Responsive - excess aldo is due to effective circulating volume depletion stimulating RAA -> aldo release
Resistant - excess aldo is not due to volume depletion |
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Treatment of Cl responsive alkalosis
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Volume administration - turn off RAA and allow bicarb excretion
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How does aldosterone contribute to Cl responsive and resistant alkalosis?
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Stimulates H+ secretion in CT
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Contraction alkalosis (2)
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Diuretics stimulate loss of Na, Cl, H2O
Same amount of bicarb but in a reduced volume |
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Cl responsive alkalosis - maintenance phase (3)
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(initiated by volume depletion -> RAA -> excess aldo)
1. AII stimulates Na/H+ exchange in PT, which increases bicarb reabsorption 2. Aldosterone stimulates H+ ATPase excreter 3. Cl- is exchanged for HCO3- in intercalated cells - REDUCED Cl- MEANS NO EXCHANGE OF Cl- in for HCO3- out |
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Alkalosis and hypokalemia (3 main phys points)
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In Cl- resistant
Excess mineralocorticoid stimulates K+ secretion in CT -> Hypokalemia Hypokalemia stimulates K+ exit from cells in exchange for H+ in, which raises plasma bicarb K+ depletion in filtrate activates H+/K+ exchanger in CT -> increased H+ secretion and bicarb reabsorption |
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Treatment of Cl resistant alkalosis
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K repletion (K-sparing diuretics)
Aldo suppression (stopping steroids, tumor resection) |
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Type B intercalated cell important mechanisms
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Cl- in and bicarb out exchanger
Cl- responsive alkalosis has Cl- deficit which reduces bicarb excretion |
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Type A intercalated cell important mechanisms
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H+ ATPase stimulated by aldosterone (in metabolic alkalosis)
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Common causes of Cl responsive alkalosis (3)
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Vomiting
NG suction Diuretics (villous ademoa, post-hypercapnia) |
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3 layers of filtration barrier - from blood to tubule
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Endothelial cell
Basement membrane Epithelial/podocyte |
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Alport syndrome (3 features)
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X-linked
Splitting and lamellation of GBM Microscopic hematuria Collagen IV mutation |
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Thin basement membrane disease (3 features)
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Defect in type IV collagen
Non-progressive hematuria EM- very thin GBM |
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Cystic renal dysplasia (4, one key histo feature)
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Sporadic/congenital/hereditary
Maldeveloped kidney Abnormal histology: CARTILAGE Common cause of childhood kidney failure |
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Progression of glomerular injury in end stage renal disease (4 steps)
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Loss of nephrons ->
Hyperfiltration and intraglomerular hypertension -> Glomerular hypertrophy and injury to endo/epithelium -> Glomerulosclerosis |
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Azotemia
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Elevation of BUN and creatinine reflecting decreased GFR
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Cortical adenoma
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Benign
Small ( < .5 cm) |
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Oncocytomas
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Benign
Large w/ granular cytoplasm (MITOCHONDRIA) |
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Angiomyolipomas
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Very large
Mesenchymal tissue w/ hemorrhage TUBEROUS SCLEROSIS |
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Renal cell carcinoma (cell type, epi, associations)
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Clear cell
Most common renal tumor in adults Associations: tobacco, Von Hippel Lindau, tuberous sclerosis |
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Hematuria, abdominal mass, flank pain, fever
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Renal cell carcinoma
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Transitional cell carcinoma (associations, presentation, flat vs papillary)
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Associations: tobacco, chemicals, chemo (cyclophosphamide), infection (schistomiasis)
Presents w/ hematuria Papillary - low grade Flat - high grade |
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Nephroblastoma/Wilms Tumor
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Most common renal malignancy in children
Derived from nephrogenic rests |
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Grade vs stage
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Grade - cytologic appearance
Stage - size and spread |
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Nephrotic syndrome definition (4)
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1. > 3.5 g/day proteinuria
2. Hypoalbuminemia < 3.5 g/day 3. Edema 4. Hyperlipidemia and lipiduria |
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What cells are damaged in nephrotic syndrome?
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Podocytes (epithelial cells)
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3 main nephrotic syndrome
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Minimal change disease
FSGS Membranous nephropathy |
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Minimal change disease (3 key features, histo, rx)
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Children
Sudden heavy proteinuria and edema Normal BP and GFR Normal histology EM - effacement of foot processes Rx - steroids |
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Focal segmental glomerulosclerosis (FSGS) (key features, histo, 2/2)
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Adults
Hypertension and decr GFR Path - focal scarring of glomeruli (segmental) 2/2 - HIV, obesity, hyperfiltration |
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Membranous nephropathy (key features, path, histo, 2/2)
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Ab-Ag complexes in subepithelial space (no inflammatory cells)
Thickened GBM w/ spikes and lumps Normal GFR 2/2 - tumors, autoimmune, infection |
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Ab-Ag complexes in subepithelial space
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Membranous nephropathy
(no inflammatory cells) |
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Secondary diseases that cause nephrotic syndrome
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Diabetic nephropathy, amyloidosis, SLE
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Diabetic nephropathy (path, key features, presentation)
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Non-enzymatic glycosylation of GBM proteins, -> thickened GBM focal/nodular glomerulosclerosis
Presentation - microalbuminuria |
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Amyloidosis
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Deposition of abnormal proteins in glomerular tufts
Congo red, birefringent apple green, fibrils AL - light chain AA - chronic infection |
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Glomerulonephritis definition (4)
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Glomerular hematuria (RBC casts and dysmorphic RBCs
Azotemia (reduced GFR) Oliguria Hypertension |
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Glomerulonephritis pathology
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Endothelial damage or immune complexes in sub endothelial space
-> inflammatory cell recruitment |
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3 primary GN disease
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post-infectious GN
membranoproliferative GN crescentic GN |
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post-stretptococcal/post-inflammatory GN (path and time course)
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Foreign Ag deposited in subendothelial space -> IgG ad complement -> neutrophils
GN 2 wks after infection |
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Membranoproliferative GN
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Chronic damage to glomerular capillary via slow deposition of Ag
Reduplication of GBM TRAM TRACKING |
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Crescentic GN (RPGN) path
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Presents as AKI
Immunologic reactions ruptures capillary wall Spreads to parietal cells of Bowman's space |
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Crescentic GN: 3 causes and distinguishing features
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ribbon-like/linear IgG - anti-GBM/Goodpasture's
granular IgG - IgA, SLE (immune complex) pauci-immune IgG - ANCA-associated disease w/ neutrophil activation |
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Secondary GN diseases
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IgA/Henoch Schonlein Purpura
Lupus nephritis |
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IgA Nephropathy/Henoch Schonlein Purpura (path)
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Most common GN in world
IgA deposition in mesangium and sub endothelial space Path - mesangioproliferative HSP - IgA deposition occurs outside kidney in skin and GI - |
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Causes of ATN (2 broad categories)
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Ischemic - low bp, low ecv, AA constriction (nsaids), EA dilation (acei, arb)
Toxic - IV contrast dye, rhabdo, heme pigments |
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ATN path (2)
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Denuded tubules
Occasional mitotic figures |
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Acute Pyelonephritis (cause, path, epi, urinalysis findings)
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Bacterial infection of renal pelvis and interstitium
Dense neutrophils w/ subcapsular abscess F > M WBC and WBC casts |
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Chronic pyelonephritis (pathogen, causes)
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Prolonged inflammatory response from kidney -> tubular atrophy and dilation (THYROIDIZATION)
Causes - recurrent acute pyelonephritis, drugs, reflux nephropathy, urinary obstruction |
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Allergic interstitial nephritis (cause, trio of presentation, histo)
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Drug exposure
Fever, rash, AKI Path - EOSINOPHILS, lymphocytes, macrophages in interstitium WBC casts and eosinophils in urine |
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Analgesic nephropathy
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Exposure to high dose phenacetin, aspirin, and caffeine
Papillary necrosis -> calcified scars |
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Multiple myeloma kidney (4 downstream effects of myeloma)
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Plasma cell tumor -> overproduction of Ig (paraproteins) ->
1. plasma cell infiltration 2. paraprotein deposition 3. amyloidosis (congo red) 4. hypercalcemia |
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Two causes of renal artery stenosis
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Atherosclerosis (90%)
Fibromuscular dysplasia (10%, women) |
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HUS/TTP (pathogen, finding)
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Infection, toxins, or enzymatic dysfunction -> endothelial damage
Schistocytes on peripheral blood smear |
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AKI definition
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Acute drop in GFR identified by rise in serum creatinine
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AKI: perfusion-related (pre renal) (3 causes, FENa?, Rx)
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Drop in Pgc -> drop in GFR
Reduced bp Constricted AA - NSAIDs Dilated EA - ACEi or ARB FENa < 1 b/c nephron is normal Rx - restore perfusion and stop meds |
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AKI: intrinsic (2 main causes and findings)
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Decreased #N
Causes: ATN, AIN ATN - muddy brown casts and high FENa |
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AKI: obstructive (post renal)
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Increased P_BS
Causes: urethra (prostate) Findings: hydroureter, hydronephrosis Rx - relieve pressure |
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Definition of chronic kidney disease (5)
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GFR < 60 OR one of following abnormalities for > 3 mo.:
1. proteinuria 2. urine sediment abnormal 3. renal imaging abnormal 4. tubular syndromes (rta, di, siadh |
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CKD Stage 1
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GFR > 90
Assess cause of kidney damage |
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CKD Stage 2
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GFR > 60
Slow rate of GFR progression |
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CKD Stage 3
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GFR > 30
Treat complications |
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CKD Stage 4
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GFR 15-29
Prepare for renal replacement |
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CKD Stage 5
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GFR < 15
Assess for renal replacement |
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Early stages of CKD: what happens as GFR declines?
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Attempts to restore GFR by dilating afferent arteriole more than efferent -> increased GFR but also release of growth factors that damage kidney
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Measures to slow CKD and GFR loss (4)
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ACEi
BP control Tobacco cessation Glycemic control in diabetics |
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What happens to GFR when you ablate a large part of the kidney?
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The decrease in GFR is not as much as expected
Due to increase in SNGFR by increased in P_GC afferent arteriole vasodilation Increased capillary pressure in glomerulus leads to sclerosis |
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CKD adaptation: Na
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More Na must be excreted by fewer nephrons
Mostly by pressure natriuresis Still most CKDers needs diuretics to prevent volume overload |
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CKD adaptation: K
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Increased K excretion is stimulated by higher aldosterone
Steady state reached at a higher K concentration, so still need to have a low K diet, K-wasting diuretics etc . . |
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CKD adaptation: acid/base (big undesired consequence?)
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As limits of ammoniagenesis are reached (~40 GFR), non-AG acidosis develops
Further fall in GFR impairs filtration of organic acids -> AG acidosis -> bone buffer releases Ca/PO4 (demineralization) |
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CKD adaptation: PTH, Ca, PO4-
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As GFR falls, more PO4- is retained ->
binds to Ca -> precipitates out and lowers serum Ca -> increase in PTH to raise serum Ca AS GFR FALLS CA AND PO4 ARE RELATIVELY NORMAL WHILE PTH INCREASES |
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CKD adaptation: Vitamin D
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Impaired synthesis -> decrease in Ca absorption from gut -> PTH
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CKD adaptation: Anemia (3 causes, Rx)
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Due to: erythropoietin deficiency
Iron deficiency Reduced RBC survival Rx - epo |
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Indications for renal replacement
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Acidosis - NaHCO3 doesnt help
Electrolytes - diuretics don't help Intoxication - stopping drugs doesnt help Overload - diuretics don't help Uremia |
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Dialysis: diffusion vs ultrafiltration
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Diffusion - movement of solute down a concentration gradient
Ultrafiltration - using pressure to push fluid (Na) through a membrane (convective clearance via dextrose) |
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Equations for MAP and CO
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MAP = CO X SVR
CO = HR X SV |
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How does volume status relate to cardiac output?
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Volume status effects pre-load, pre-load effects stroke volume and CO = HR X SV
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Main defect in essential hypertension?
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Pressure natriuresis
High blood pressure is not corrected by dumping Na into urine |
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How does kidney disease cause secondary HTN?
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Impaired Na excretion -> volume overload -> HTN
Correct w/ diuretics and diet restriction |
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How does renal artery stenosis cause secondary HTN?
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Stenosis -> low ECV -> angiotensin II -> Na retention + loss of pressure natriuresis
Increases GFR and Na retention in uncompromised kidney |
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How can tumors cause hypertension?
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1. Secrete aldo -> Na retention, hypokalemia, metabolic alkalosis NO EDEMA DUE TO ALDO ESCAPE
2. pheochromocytomas -> secrete catecholamines -> increased SVR -> incr MAP + RAA activation -> HTN |
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Pharm: how to lower intravascular volume?
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Diuretics
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Pharm: how to reduce venous tone?
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NO derivatives and dihydrop Ca channel blockers
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Main targets for hypertension pharm? (4)
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Lower intravascular volume - diuretics
Reduce venous tone - NO, CCBs Reduce HR - beta blockers Block SNS - alpha agonists |
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Pharm: how to reduce heart rate?
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Beta blockers and non-dihydrop CCBs
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Pharm: how to lower SNS tone
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Alpha2 agonists - dilate arterioles
Alpha1 agonists - peripheral |
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Diuretics complications (5)
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Impotence
New onset DM Worse lipid profile Gout Hypokalemia |
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ACEi and ARB complications
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Cough due to increased bradykinin
Hypotension Hyperkalemia CKD progression Not in pregnancy |
