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1IBSNBDPMPHZ▯PG▯$,% Nicolette Wong nsw20@ic.ac.uk0#+&$5*7&4▯ • Identify the functions of the kidney • Understand the pathophysiology of chronic kidney disease • Apply the knowledge of kidney function to the complications of chronic kidney disease • Differentiate between drugs that: • Are nephrotoxic • Affect serum creatinine • Treat the kidneys in CKD • Reduce cardiovascular risk in CKD$POUFOU▯ • The 9 core drugs • Anatomy • Functions of the kidney • Overview of CKD • Drugs that harm the kidney • Drugs that influence creatinine • Drugs that help the kidney • Drugs that reduce cardiovascular risk • Menti5IF▯▯▯DPSF▯ESVHT Drugs that harm the kidney Drugs that help the kidney 1. Gentamicin (antibiotic) 4. Calcium channel blockers 2. NSAIDs 5. ACE inhibitors 6. Angiontensin receptor blockers 7. Dapagliflozin (SGLT-2 inhibitor) Drug that influences creatinine Drugs that reduce cardiovascular risk 3. Trimethoprim (antibiotic) 8. Aspirin 9. Statins.FOUJ4#"▯▯▯ Q1: Marshall, a 62-year-old male, is diagnosed at the GP with chronic kidney disease. Which of the following symptoms might he have experienced? A. Facial erythema B. Oedema C. Muscular hypertonicity D. Hypotension E. Increased appetite4#"▯▯▯▯"/48&3 Q1: Marshall, a 62-year-old male, is diagnosed at the GP with chronic kidney disease. Which of the following symptoms might he have experienced? A. Facial erythema → Should be pallor B. Oedema C. Muscular hypertonicity → Should be muscle cramps D. Hypotension → Should be hypertension E. Increased appetite → Should be decreased appetite"OBUPNZ▯▯ Renal pyramid .BUDI▯UIF▯GVODUJPOT▯PG▯UIF▯LJEOFZ▯ 1. Waste excretion Retain bicarbonate or excrete acid 2. Reabsorption of nutrients To adjust Na levels, controls renin release which affects angiotensin II and aldosterone Urea, creatinine, uric acid, drugs and their 3. Maintaining pH metabolites 4. Osmolality regulation Erythropoietin, renin and calcitriol ADH regulates aquaporin and UT receptor 5. Regulating blood pressure expression Glucose, amino acids, water, bicarbonate, 6. Secretion of active compounds phosphates, Cl-, Na+, Mg2+ & K+ 'VODUJPOT▯PG▯UIF▯LJEOFZ WORRMS 1. Waste excretion Removal of urea (protein breakdown), creatinine, uric acid (nucleic acid breakdown), drugs and their metabolites 2. Reabsorption of nutrients Reabsorption of glucose, amino acids, water, bicarbonate, phosphates, Cl-, Na+, Mg2+ & K+ Retains bicarbonate in a state of acidemia or 3. Maintaining pH excretes acid in a state of alkalemia ADH regulates aquaporin and UT receptor expression, 4. Osmolality regulation controlling water reabsorption (eg. ↑ during dehydration) To adjust Na levels, kidneys regulate renin release which 5. Regulating blood pressure affects angiotensin II and aldosterone, altering BP Secretes erythropoietin (produces RBC), renin (affects BP) 6. Secretion of active compounds and calcitriol (active Vit D, controls Ca2+ and PO43-)",*▯WT▯$,% Acute Kidney Injury Chronic Kidney Disease • Rapid rate of deterioration • Slow rate of deterioration • Caused by injury, medication, or • Caused by high blood pressure, illness diabetes, and an inflammatory • Typically normal sized kidneys condition (glomerulonephritis) • Typically small kidneys$ISPOJD▯LJEOFZ▯EJTFBTF Definition Causes • Abnormalities of kidney structure • Diabetes or function, present for ≥3 • Hypertension months, with implications for health • Age-related decline • Proteinuria or haematuria, and/or • Glomerulonephritis a reduction in the glomerular filtration rate • Polycystic kidney disease • Medications such as • NSAIDs • Gentamicin • Proton pump inhibitors • Lithium ,FZ▯EFGJOJUJPOT Term Definition Clinical significance Estimated glomerular A measurement of how well Low eGFR = kidney disease, followed by kidney failure. filtration rate (eGFR) kidneys are filtering blood, based An eGFR<60 for 3 months or more, or an eGFR above 60 on a patient's serum creatinine with kidney damage (marked by high levels of albumin in level, age, sex and race. your urine) means CKD Proteinuria An excess of protein (usually Marker of glomerular dysfunction- Protein (albumin) albumin) in the urine passes through glomerular membrane Haematuria Blood in the urine Marker of glomerular dysfunction- RBCs pass through glomerular membrane Urea A substance formed by the Increased plasma urea indicates kidney damage breakdown of protein in the liver Creatinine A waste product produced by Increased plasma creatinine indicates kidney damage muscles, freely filtered in kidneys Albumin creatinine The ratio of albumin to creatinine High ACR = high albumin = proteinuria = kidney disease ratio (ACR) in the urine1BUIPQIZTJPMPHZ In response to renal injury, there is an… • Increase in intra-glomerular pressure as the kidney tries to maintain constant glomerular filtration • Increase in glomerular permeability to macro-molecules (eg. protein) may result in glomerular inflammation, fibrosis, and scarring • Increase in angiotensin II production Causing progressive renal scarring and loss of kidney function.$MJOJDBM▯GFBUVSFT • Usually asymptomatic Uremia: “urine in the blood” • Pruritus (itching) → Uremia Build up of harmful waste products • Loss of appetite → Uremia in the blood (eg. urea) • Nausea → Uremia • Oedema → Decreased removal of excess fluid from body (low GFR) • Muscle cramps → Uremia • Peripheral neuropathy → Uremia • Pallor → Low EPO = anaemia • Hypertension → Upregulation of RAAS, promoting salt and water retention Cardiovascular disease Oedema Protein malnutrition Hyperkalaemia $PNQMJDBUJPOT Uremia Removal of urea (protein breakdown), creatinine, uric acid 1. Waste excretion (nucleic acid breakdown), drugs and their metabolites Reabsorption of glucose, amino acids, water, bicarbonate, 2. Reabsorption of nutrients phosphates, Cl-, Na+, Mg2+ & K+ 3. Maintaining pH Metabolic acidosis Retains bicarbonate in a state of acidemia or excretes bicarbonate in a state of alkalemia 4. Osmolality regulation ADH regulates aquaporin and UT receptor expression, controlling water reabsorption (eg. ↑ during dehydration) To adjust Na levels, kidneys regulate renin release which 5. Regulating blood pressure affects angiotensin II and aldosterone, altering BP Anaemia Secretes erythropoietin (produces RBC), renin (affects BP) 6. Secretion of active compounds and calcitriol (active Vit D, controls Ca2+ and PO43-) Renal osteodystrophy$PNQMJDBUJPOT • Anaemia • Renal osteodystrophy • Cardiovascular disease • Protein malnutrition • Metabolic acidosis • Hyperkalaemia • Pulmonary oedema%SVHT▯UIBU▯IBSN▯ UIF▯LJEOFZ▯ OFQISPUPYJD 1. Gentamicin (antibiotic) 2. NSAIDs"OUJCJPUJDT▯▯(FOUBNJDJO What is its MOA? How does it contribute to CKD? Aminoglycoside antibiotic Targets PCT epithelial cells in the Bactericidal renal cortex Binds to the bacterial 30S ribosomal subunit disturbing the translation of mRNA leading to the formation of dysfunctional Inhibits protein synthesis in renal cells proteins Necrosis of renal cells in PCT (Acute tubular necrosis) Acute Kidney Failure/4"*%T What is its MOA? How does it contribute to CKD? • NSAIDs inhibit the COX enzyme, decreasing production of Decreased prostaglandins prostaglandins & thromboxanes, reducing inflammation Inhibition of vasodilation • 👍 COX-2, 👎 COX-1 Vasoconstriction of afferent arteriole Reduced renal blood flow, reduced GFR Acute Kidney Failure /FQISPUPYJD▯ESVHT▯▯4VNNBSZ Drug class Example Target MOA Side effects Effect on kidneys Antibiotics Gentamicin 30s Binds to the bacterial 30s ribosomal Ototoxicity and Inhibits protein synthesis (Aminoglycoside) ribosomal subunit disturbing the translation of mRNA nephrotoxicity in renal cells, resulting in subunit leading to the formation of dysfunctional acute tubular necrosis, in bacteria proteins followed by acute renal failure NSAIDs Ibuprofen, Cyclo- NSAIDs inhibit the COX enzyme, decreasing GI: irritation, Prolonged analgesic abuse naproxen, oxygenase production of prostaglandins & ulceration, is associated with chronic diclofenac (COX) thromboxanes, reducing inflammation perforation renal failure. enzyme 👍 COX-2, 👎 COX-1 CV: stroke, MI, Inhibits PG synthesis and hypertension reduces renal blood flow Reduced creatinine clearance and possible nephritis4#"▯▯▯ Q2: Which of the following most accurately describes the mechanism by which NSAIDs are nephrotoxic? A. Inhibit the production of thromboxane A2 B. Increase the production of thromboxane A2 C. Act on the COX-1 enzyme D. Inhibit the production of prostaglandins E. Increase the production of prostaglandins4#"▯▯▯ Q2: Which of the following most accurately describes the mechanism by which NSAIDs are nephrotoxic? A. Inhibit the production of thromboxane A2 → reduces platelet aggregation B. Increase the production of thromboxane A2 C. Act on the COX-1 enzyme → reduces protection in gastric mucosa from acid D. Inhibit the production of prostaglandins E. Increase the production of prostaglandins%SVH▯UIBU▯JOGMVFODFT▯ DSFBUJOJOF 3. Trimethoprim (antibiotic)%SVH▯UIBU▯JOGMVFODFT▯DSFBUJOJOF Trimethoprim • Competitive inhibition of tubular secretion of creatinine • Increased serum creatinine • (eGFR equation dependent on serum creatinine) INCREASED • eGFR would appear lowered SERUM • But does not signify a deterioration in CREATININE renal function Trimethoprim breaks the link between creatinine and GFR %SVH▯UIBU▯JOGMVFODFT▯DSFBUJOJOF Drug class Example Target MOA Side effects Effect on kidneys Antibiotic Trimethoprim Dihydrofolate Inhibits the reduction of dihydrofolic acid Diarrhoea It inhibits the active (Anti-folate) reductase to tetrahydrofolic acid (active form) – a Skin reactions secretion of enzyme necessary component for synthesising Affects GFR value creatinine so the in bacteria purines required for DNA and protein equation to calculate production (by bacteria) GFR is now invalid. Trimethoprim inhibits the production of It breaks the link folic acid by bacteria, which is necessary for between creatinine survival. and GFR*OWFTUJHBUJPOT • eGFR: checked using U&Es. Two tests are required 3 months apart to confirm a diagnosis of chronic kidney disease • Proteinuria: checked using a urine albumin:creatinine ratio (ACR) • Haematuria: checked using a urine dipstick • Renal ultrasound: check for accelerated CKD, haematuria, family history of polycystic kidney disease or evidence of obstruction.BOBHFNFOU▯ Aims 1. Slow the progression of the disease 2. Reduce the risk of cardiovascular disease 3. Reduce the risk of complications 4. Treating complications.BOBHFNFOU▯ Aims 1. Slow the progression of the disease • Optimise diabetic control • Optimise hypertensive control • Treat glomerulonephritis 2. Reduce the risk of cardiovascular disease 3. Reduce the risk of complications 4. Treating complications %SVHT▯UIBU▯IFMQ▯ UIF▯LJEOFZ 4. Calcium channel blockers 5. ACE inhibitors 1 line or 6. Angiotensin receptor blockers 7. Dapagliflozin (SGLT-2 inhibitor) Aim: reduce glomerular hypertension$BMDJVN▯DIBOOFM▯CMPDLFST▯ $$#T What is its MOA? How does it treat CKD? Blood pressure control Blocks L-type Ca channels on vascular 2+ smooth muscle CaCCB slows the progression of kidney disease, and 2+ improves cardiovascular Decreases Ca influx, inhibiting contraction (vascular constriction) and renal outcomes Resultant vasodilation reduces peripheral resistance Lowers blood pressure4PNF▯DMBSJGJDBUJPOT▯▯ The site of vasodilation matters Peripheral vasodilation = decreased blood pressure = decreased glomerular pressure Renal vasodilation = increased glomerular pressure GFR vs eGFR GFR: the rate of blood flow through the kidneys eGFR: a measure of kidney function, based on serum creatinine (Low eGFR = high serum creatinine) Low eGFR has several causes and does not mean low glomerular pressure Low eGFR can be caused by: 1. Vasoconstriction of afferent arteriole 2. Glomerular hypertension4PNF▯DMBSJGJDBUJPOT▯ Does vasodilating the afferent arteriole increase or decrease glomerular pressure? Vasodilating = increases glomerular pressure Vasoconstricting = decreases glomerular pressure4PNF▯DMBSJGJDBUJPOT▯ Does vasodilating the afferent arteriole increase or decrease glomerular pressure?3FOJO▯BOHJPUFOTJO▯BMEPTUFSPOF▯TZTUFN Angiotensin TWO TIGHTENS 1 4 RAAS is found in many tissues, 2 including heart, brain, vascular 3 and renal tissues. 3 2 4 4 5 53FOJO▯BOHJPUFOTJO▯BMEPTUFSPOF▯TZTUFN RAAS is found in many tissues, including heart, brain, vascular and renal tissues."$&▯JOIJCJUPST What is its MOA? How does it treat CKD? Inhibits the angiotensin converting Blood pressure control slows the enzyme (ACE) progression of kidney disease, and improves cardiovascular and renal Prevents the conversion of angiotensin-I outcomes to angiotensin II by ACE Prevents downstream vasoconstrictive Prevents downstream release of aldosterone, effects of angiotensin II promoting renal excretion of sodium and water Vasodilation Lowers blood pressure Lowers blood pressure &YQMBJO▯UIJT▯DPOUSBEJDUJPO▯ Treatment aim: Vasoconstrict afferent arteriole to reduce glomerular pressure But ACE inhibitors vasodilate! How does that work?? ACE inhibitors vasodilate both afferent and efferent arteriole but it has a preferential vasodilation of the renal efferent arteriole&YQMBJO▯UIJT▯DPOUSBEJDUJPO▯ How do ACE inhibitors both harm the kidney and treat CKD? Harm the kidneys – hyperkalaemia and lowers eGFR 1. Aldosterone retains sodium and excretes potassium No more aldosterone = too much potassium in blood so hyperkalaemia 2. Decreased renal perfusion pressure decreases glomerular filtration, which impairs the kidney's ability to compensate for low perfusion states eGFR and serum potassium must be regularly monitored"OHJPUFOTJO▯SFDFQUPS▯CMPDLFST▯ "3#T What is its MOA? How does it treat CKD? Non-competitive antagonist of the Blood pressure control slows the angiotensin II type 1 (AT-1) receptor on progression of kidney disease, and kidneys and vasculature improves cardiovascular and renal outcomes Prevents downstream vasoconstrictive Prevents downstream release of aldosterone, effects of angiotensin II promoting renal excretion of sodium and water Vasodilation Lowers blood pressure Lowers blood pressure Workvasodilates efferent > afferent,4(-5▯▯▯JOIJCJUPST▯▯%BQBHMJGMP[JO What is its MOA? Reversibly inhibits sodium-glucose co- transporter 2 (SGLT-2) in the renal PCT Reduces glucose and sodium reabsorption (from urine to blood) and increases excretion Increased natriuresis normalises tubuloglomerular feedback Reduced intra-glomerular hypertension Decreases proteinuria4(-5▯▯▯JOIJCJUPST▯▯%BQBHMJGMP[JO Tubuloglomerular feedback4(-5▯▯▯JOIJCJUPST▯▯%BQBHMJGMP[JO 1. More salt in pee in PCT 2. More salt in the pee that reaches the DCT, where the macula densa is 3. Increased salt concentration in tubule reaching the macula densa 4. Mesangial cells detect high sodium uptake 5. Causes contraction of the afferent arteriole and a reduction in GFR How does it treat CKD? If body detects salty pee, thinks person is Prevents decline in kidney function dehydrated. Wants to retain more water, so will hypertension mediated throughar contract afferent arteriole to prevent filtration. of its effect on glycemic controldent&YQMBJO▯UIJT▯DPOUSBEJDUJPO▯ If CKD is characterised by low eGFR, why are we trying to reduce it further? Drugs that treat CKD will reduce eGFR acutely, but over time, it prevents further decline in kidney function and eGFR %SVHT▯UIBU▯IFMQ▯UIF▯LJEOFZT Drug class Example Target MOA Side effects Effect on Aim: improve proteinuria kidneys Calcium Amlodipine L-type calcium Blocks L-type calcium channels on Ankle oedema, Prevents channel Calcium channel blockchannel vascular smooth muscle. This ↓ Ca2+ Constipation, Palpitations kidney damage blockers on vascular smooth influx. The resultant vasodilation Flushing/Headaches associated with • ACE inhibitors muscle reduces peripheral resistance. (caused by vasodilation!) high BP ACE • Angiotensin receptor blockerssin Inhibit the angiotensin converting Cough, Hypotension Prevents inhibitors converting enzyme enzyme. HyperDiagram / picsal kidney damage Prevent the conversion of angiotensin I Injury, Renal failure (in associated with • SGLT-2 inhibitors: Dapagliflozi to angiotensin II by ACE. renal artery stenosis), high BP Urticaria/Angioedema • Aspirin Angiotensin Candesartan Angiotensin Non-competitive antagonist at AT1 Hypotension, Prevents receptor receptor receptor (on kidneys and vasculature), Hyperkalaemia, Foetal kidney damage blockers found on kidneys blocking the action of angiotensin II injury, Renal failure (in associated with and vasculature renal artery stenosis) high BP SGLT-2 Dapagliflozin Sodium-glucose co- Reversibly inhibits SGLT-2 in the renal Uro-genital infections (↑ Improves inhibitors transporter 2 PCT to reduce sodium and glucose glu), ↓ bone formation proteinuria in PCT in the kidney reabsorption and increase excretion. Can worsen DKA4#"▯▯▯ Q3: Which of the following is the target of losartan? A A. A D B. B B C. C C E D. D E. E D4#"▯▯▯▯"/48&3 Q3: Which of the following is the target of losartan? A D ARB: A. A Non-competitive B. B B antagonist of the angiotensin II C. C type 1 (AT-1) C E receptor on D. D kidneys and E. E vasculature D.BOBHFNFOU▯ Aims 1. Slow the progression of the disease 2. Reduce the risk of cardiovascular disease 3. Reduce the risk of complications 4. Treating complications)PX▯EPFT▯$,%▯JODSFBTF▯$7%▯SJTL CKD causes a systemic, chronic proinflammatory state contributing to vascular and myocardial remodelling processes resulting in CVD caused by- eg. atherosclerotic lesions & vascular calcification Why do I care? Cardiovascular disease (CVD) is the primary cause of morbidity and mortality in chronic kidney disease (CKD)%SVHT▯UIBU▯SFEVDF▯ DBSEJPWBTDVMBS▯SJTL 8. Aspirin 9. Statins/4"*%T▯▯"TQJSJO What is its MOA? How does it reduce CV risk? (Low dose aspirin) • Irreversible inactivation of COX enzyme • Reduces the risk of atherothrombosis • Prevents oxidation of arachidonic acid to produce Aspirin prostaglandins • Reduction of thromboxane A2 in platelets reduces aggregation&YQMBJO▯UIJT▯DPOUSBEJDUJPO▯ Aspirin (an NSAID), can be used NSAIDs are nephrotoxic VS as part of CKD treatment The benefits outweigh the costs Studies show that aspirin does not significantly affect renal function in CKD patients Aspirin can reduce the risk of CVD BUT in general, we tend to avoid aspirin for primary prevention4UBUJOT What is its MOA? How does it reduce CV risk? Competitive inhibitor of HMG-CoA • Reduces the amount of atheroma reductase, which converts HMG- deposits in arteries and stops any CoA to mevalonate in the further atheroma deposition cholesterol synthesis pathway, • Makes existing deposits less likely reducing cholesterol synthesis to break off and cause a thrombosis %SVHT▯UIBU▯SFEVDF▯DBSEJPWBTDVMBS▯SJTL Drug Aim: improve proteinuriarget MOA Side effects Effect on kidneys Anti- Aspirin Cyclo-oxygenase Irreversible inactivation of COX enzyme. Dyspepsia Reduces plate•ts/ alcium ch aCnX)nenzlmbeloc Pkrvernts oxidation of arachidonic acid to Haemorrhage cardiovascular risk NSAIDs produce prostaglandins. • ACE inhibitors Reduction of thromboxane A2 in platelets reduces aggregation. • Angiotensin receptor blockers Reduction of PGE2 (i) at sensory pain neurones reduces pain and sensation and • SGLT-2 inhibitors: Dapagliflozin (ii) in the brain decreases fever. Statins Atorvastatin HMG-CoA Competitive inhibitor of HMG-CoA Muscle toxicity, Reduces • Aspirin reductase in the reductase, which converts HMG-CoA to GI effects: cardiovascular risk liver mevalonate in the cholesterol synthesis constipation, pathway, reducing cholesterol synthesis diarrhoea74"2▯▯▯ Q4: What is the common cause of pruritus, loss of appetite, nausea, muscle cramps and peripheral neuropathy in CKD?74"2▯▯▯ Q4: What is the common cause of pruritus, loss of appetite, nausea, muscle cramps and peripheral neuropathy in CKD? Uremia • “urine in the blood” • Build up of harmful waste products in the blood (eg. urea)4#"▯▯▯ Q5: Which group of medications treats CKD by reducing glomerular hypertension? A. CCBs, Statins, Dapagliflozin B. SGLT-2 inhibitors, ARBs, Gentamicin C. Aspirin, ACE inhibitors, CCBs D. Gentamicin, NSAIDs, SGLT-2 inhibitors E. ACE inhibitors, Dapagliflozin, ARBs4#"▯▯▯ Q5: Which group of medications treat CKD by reducing glomerular hypertension? A. CCBs, Statins, Dapagliflozin B. SGLT-2 inhibitors, ARBs, Gentamicin C. Aspirin, ACE inhibitors, CCBs D. Gentamicin, NSAIDs, SGLT-2 inhibitors E. ACE inhibitors, Dapagliflozin, ARBs 46.."3:▯▯▯▯$PSF▯%SVHT Treats CKD Nephrotoxic • Gentamicin Nephroprotective Reduces CVD risk Causes necrosis of renal cells in the PCT • CCBs • Aspirin • NSAIDs peripheral vasodilationing Inhibits thromboxane A2 Decreases prostaglandins, production, decreasing causing vasoconstriction • AInhibits ACE, decreasing platelet aggregation angiotensin II, causing vasodilation (efferent > afferent) • Statins Influences creatinine • ARBs Reduces the amount of Non-competitive antagonist of arteries deposits in • Trimethoprim AT-1, decreasing angiotensin II, Inhibits tubular secretion of creatinine, afferent)asodilation (efferent > increasing serum creatinine • Dapagliflozin natiuresis and tubuloglomerular feedback, causing afferent vasoconstriction46.."3:▯▯▯▯$MBSJGJDBUJPOT The site of vasodilation ACEi and ARBs matters: Low eGFR has several preferentially vasodilate Peripheral = decreased causes and does not glomerular pressure, mean low glomerular the efferent arteriole, Renal = increased pressure decreasing glomerular glomerular pressure pressure GFR vs eGFR Vasodilating the afferent Drugs that treat CKD will GFR: rate of blood flow acutely reduce eGFR but eGFR: measures kidney arteriole increases will prevent decline in function with serum glomerular pressure & kidney function and creatinine vice versa eGFR over time 5)"/,▯:06▯ Please fill in the Feedback form! Name: Nicolette Wong Email: nsw20@ic.ac.uk https://app.medall.org/training/feedback/anonymous?keyword=d15e39e164 4cd514deaa49e0&organisation=imperial-pharmacology-society3FTPVSDFT▯ .BUDI▯UIF▯GVODUJPOT▯PG▯UIF▯LJEOFZ▯ 1. Waste excretion Retain bicarbonate or excrete acid 2. Reabsorption of nutrients To adjust Na levels, controls renin release which affects angiotensin II and aldosterone Urea, creatinine, uric acid, drugs and their 3. Maintaining pH metabolites 4. Osmolality regulation Erythropoietin, renin and calcitriol ADH regulates aquaporin and UT receptor 5. Regulating blood pressure expression Glucose, amino acids, water, bicarbonate, 6. Secretion of active compounds phosphates, Cl-, Na+, Mg2+ & K+ /FQISPUPYJD▯ESVHT Drug class Example Target MOA Side effects Effect on kidneys Antibiotics (Aminoglycoside) NSAIDs %SVH▯UIBU▯JOGMVFODFT▯DSFBUJOJOF Drug class Example Target MOA Side effects Effect on kidneys Antibiotic (Anti-folate) %SVHT▯UIBU▯IFMQ▯UIF▯LJEOFZT Drug class Example Target MOA Side effects Effect on kidneys Calcium channel blockers ACE inhibitors Angiotensin receptor blockers SGLT-2 inhibitors %SVHT▯UIBU▯SFEVDF▯DBSEJPWBTDVMBS▯SJTL Drug class Example Target MOA Side effects Effect on kidneys Anti- platelets/ NSAIDs Statins