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Waste filtration, electrolyte balancing, blood pressure management, hormone generation, and acid-base maintenance are just a few of the vital roles the kidneys play in preserving general health. Nephrotoxicity, which can result in diseases like acute kidney injury (AKI) and chronic kidney disease (CKD), is the term used to describe kidney damage brought on by dangerous substances including medications, chemicals, and poisons. Numerous chemical and pharmaceutical compounds are linked to various kidney illnesses, such as kidney stones, glomerulonephritis, interstitial nephritis, and nephrotic syndrome. ACE inhibitors, diuretics, immunosuppressants, phosphate binders, and erythropoiesis-stimulating medicines are among the drugs used to treat kidney illnesses, depending on the stage and kind of kidney impairment. In order to improve patient outcomes and stop more kidney damage, early diagnosis and treatment are essential. This article lists the main reasons, kidney disease phases and treatment choices, with an emphasis on the effects of nephrotoxins and therapeutic strategies for different renal disorders.
An essential component of the human body, the kidneys are necessary for preserving general health. They are fist-sized, bean-shaped structures that are situated directly below the rib cage on either side of the spine. Nephrons, which are microscopic filtering units, number around a million in each kidney. The main job of the kidneys is to filter blood, eliminating waste, toxins, and extra fluid, which is then expelled from the body as urine. Apart from their filtering function, the kidneys also control vital body processes like:
Electrolyte and fluid balance: They make sure the body keeps the right amounts of potassium, sodium, and other electrolytes, which are necessary for the normal operation of muscles and nerves.
Regulating Blood Pressure Regulation: By controlling fluid balance and releasing hormones like renin, the kidneys aid in blood pressure maintenance.
Hormone creation: They oversee creating hormones such as calcitriol, an active form of vitamin D that aids in controlling calcium levels, and erythropoietin, which promotes the creation of red blood cells.
Maintaining Acid-Base Balance: By removing hydrogen ions and reabsorbing bicarbonate, the kidneys assist in keeping the pH of the body within a normal range. [1]
Fig 1. Normal Kidney.
Nephrotoxicity:
The term "nephrotoxicity" describes damage to the kidneys or reduced renal function brought on by exposure to hazardous substances, chemicals, medications, or other factors. It can result in either short-term or long-term renal dysfunction, which impacts the kidneys' capacity to filter waste, maintain fluid and electrolyte balance, and control blood pressure.
Fig 2. Stages of Chronic Kidney Disease
Chemical And Drug Agent Leads to Different Types of Kidney Disease
Exposure to certain substances, poisons, or medications can cause various kidney disorders. The following is a list of kidney illnesses, along with the chemicals and medications that are known to cause or worsen them:
1. Acute Kidney Injury (AKI)
AKI is a sudden loss of kidney function, often reversible if the cause is removed.
Flavonoids, lignans, alkaloids, and tannins are examples of active compounds.
Mechanism: It has been demonstrated to prevent kidney damage by lowering oxidative stress and inflammation. It is well-known for its diuretic, anti-inflammatory, and antioxidant qualities. Traditional medicine frequently uses it to treat kidney stones and maintain renal function.
Research: By lowering oxidative stress, apoptosis, and inflammation in kidney tissues, Phyllanthus niruri may be able to lessen renal toxicity brought on by nephrotoxic substances like gentamicin. [44–45]
2. Withania somnifera (Ashwagandha)
Alkaloids and withanolides are active compounds.
Mechanism: Ashwagandha's anti-inflammatory and antioxidant qualities help lessen kidney damage brought on by inflammation and free radicals. It could help improve renal blood flow by controlling nitric oxide levels.
Research: By reducing blood creatinine and BUN levels, Withania somnifera has been demonstrated to enhance renal function and lessen gentamicin-induced nephrotoxicity in animal models. [46–48]
3. Cichorium intybus (Chicory)
Flavonoids, tannins, alkaloids, and inulin are the active ingredients.
Mechanism: Chicory helps to preserve renal function and lessen oxidative stress because of its diuretic, anti-inflammatory, and antioxidant properties.
Research: By minimizing renal damage brought on by harmful substances, studies indicate that Cichorium intybus improves kidney health and lessens the effects of cadmium-induced nephrotoxicity. [49–50]
4. Curcuma longa (Turmeric)
One of the active ingredients is curcumin, a polyphenolic molecule.
Mechanism: Curcumin has strong anti-inflammatory and antioxidant properties. It aids in lowering inflammation and oxidative stress, two factors that frequently lead to nephrotoxicity. Additionally, it has been demonstrated to stop cellular apoptosis and kidney fibrosis.
Research: By lowering indicators of oxidative stress and enhancing kidney function, Curcuma longa has shown protective benefits in cisplatin-induced nephrotoxicity and lead-induced nephropathy. [51–52]
5. Boswellia serrata (Indian Frankincense)
The active ingredients are boswellic acids.
Mechanism: Pro-inflammatory cytokines like TNF-α and IL-6 are known to be inhibited by boswellic acids, which also have anti-inflammatory and antioxidant qualities. It also aids in preventing toxins from harming kidney cells.
Research: By lowering oxidative stress and renal inflammation, Boswellia serrata can guard against NSAID-induced nephrotoxicity. [53–54]
6. Azadirachta indica (Neem)
Flavonoids, nimbidin, and azadirachtin are the active ingredients.
Mechanism: Neem has long been utilized as a cleansing, anti-inflammatory, and antioxidant. It can improve renal healing processes and lessen oxidative damage and inflammation in the kidneys.
Research: By lowering blood creatinine, urea levels, and kidney histopathological damage, neem extracts have been demonstrated to mitigate diabetic nephropathy and gentamicin-induced nephrotoxicity. [55–56]
7. Silybum marianum (Milk Thistle)
Active Compounds: Silymarin (a flavonoid complex).
Mechanism: Silymarin is a potent antioxidant that protects liver and kidney cells from oxidative damage. It helps stabilize cell membranes, regenerate damaged tissues, and reduce inflammation.
Research: Silybum marianum has shown nephroprotective effects in various animal models, particularly in preventing cisplatin-induced nephrotoxicity, by decreasing oxidative stress and improving kidney function markers. [57-58]
8. Tribulus terrestris (Puncture Vine)
Alkaloids, steroids, flavonoids, and saponins are examples of active compounds.
Mechanism: Tribulus terrestris, which is well-known for its diuretic, anti-inflammatory, and antioxidant qualities, protects the kidneys by preventing oxidative damage and preserving renal function.
Research: By lowering blood creatinine and raising antioxidant levels in the kidneys, Tribulus terrestris can prevent gentamicin-induced nephrotoxicity, according to animal experiments. [59–60]
9. Allium sativum (Garlic)
Flavonoids, sulfur compounds, and allicin are the active ingredients.
Mechanism: Garlic's anti-inflammatory and antioxidant qualities are well-known. Additionally, it enhances renal function and lessens oxidative stress in the kidneys.
Research: Garlic's antioxidant qualities and ability to increase renal blood flow may help reduce drug-induced nephrotoxicity, especially that brought on by gentamicin. [61–62]
10. Ginkgo biloba (Ginkgo)
Flavonoids and terpenoids (ginkgolides) are active compounds.
Mechanism: Ginkgo, a potent antioxidant, lowers inflammation and increases circulation, all of which can help shield the kidneys from harm.
Research: Ginkgo biloba can improve kidney function indicators and lessen oxidative damage by protecting against gentamicin-induced nephrotoxicity, according to animal studies. [63–64]
11. Hibiscus rosa-sinensis (Hibiscus)
Organic acids, flavonoids, and anthocyanins are examples of active compounds.
Mechanism: Hibiscus, which is well-known for its anti-inflammatory and antioxidant properties, aids in reducing kidney damage brought on by inflammation and oxidative stress.
Research shows that Hibiscus rosa-sinensis can lessen the effects of nephrotoxicity caused by ethylene glycol by lowering histopathological damage and serum creatinine. [65–66]
12. Glycyrrhiza glabra (Licorice)
Triterpenoids, flavonoids, and glycyrrhizin are the active ingredients.
Mechanism: Strong anti-inflammatory, anti-fibrotic, and antioxidant qualities of licorice help shield kidney tissues against fibrosis and injury.
Research: In models produced by gentamicin and cisplatin, licorice extracts have demonstrated nephroprotective efficacy against drug-induced nephrotoxicity. [67–68]
13. Glycyrrhiza uralensis (Chinese Licorice)
Glycyrrhizin, glycyrrhetic acid, and flavonoids are the active ingredients.
Mechanism: Glycyrrhiza uralensis, which is well-known for its hepatoprotective, antioxidant, and anti-inflammatory qualities, provides defense against kidney damage brought on by inflammation and oxidative stress.
Research: It has been demonstrated to improve renal function and shield the kidneys from oxidative stress by reducing cyclophosphamide-induced nephrotoxicity. [69–70]
14. Moringa oleifera (Drumstick Tree)
Vitamins, polyphenols, and flavonoids are examples of active compounds.
Mechanism: The anti-inflammatory and antioxidant qualities of moringa help shield the kidneys from oxidative stress and pollutants.
Research: In animal models of diabetic nephropathy and gentamicin-induced nephrotoxicity, Moringa oleifera has demonstrated nephroprotective properties, lowering renal damage and enhancing kidney function. [71–73]
15. Pterocarpus marsupium (Indian Kino Tree)
Pterocarpin, marsupin, and tannins are the active ingredients.
Mechanism: This plant, which is well-known for its anti-inflammatory and antioxidant properties, aids in shielding the kidneys from harm caused by free radicals.
Research: By lowering oxidative stress and kidney damage, Pterocarpus marsupium can guard against cisplatin-induced nephrotoxicity. [74–76]
Semi Synthetic Products for Nephrotoxicity:
1. Acetaminophen (Paracetamol) Derivatives
Compound Semi-Synthetic: N-acetylcysteine (NAC)
Mechanism: The amino acid cysteine is the semi-synthetic precursor of NAC. It serves as a precursor to glutathione, a potent antioxidant that aids in the kidneys' detoxification of reactive oxygen species (ROS). By restoring glutathione levels and halting oxidative damage, NAC is used therapeutically to treat acute kidney injury (AKI) and acetaminophen-induced nephrotoxicity.
Research: According to a number of studies, NAC can help lessen kidney damage brought on by nephrotoxic medications like gentamicin and cisplatin. [77–78]
2. Doxorubicin Derivatives
Doxorubicin (Doxil), a semi-synthetic compound, is liposomal
Mechanism: A modified form of doxorubicin, liposomal doxorubicin is encapsulated in liposomes to increase its therapeutic index and lessen nephrotoxicity. Liposomal formulations prevent harm to non-target organs, such as the kidneys, while assisting in the drug's targeting of cancer cells.
Research: Compared to standard doxorubicin, which is known to cause nephrotoxicity, liposomal doxorubicin has demonstrated less renal toxicity. [79–80]
3. Penicillin Derivatives
Amoxicillin and ampicillin are semi-synthetic compounds.
Mechanism: Semi-synthetic derivatives of penicillin, ampicillin and amoxicillin have altered side chains that contribute to their broader range of activity. These semi-synthetic antibiotics have a reduced nephrotoxic profile and are less likely to harm kidneys when used in clinical settings, even though penicillin itself can result in drug-induced nephrotoxicity.
Research: When compared to previous penicillin derivatives, studies have shown that amoxicillin has a superior safety profile with less nephrotoxicity. [81–82]
4. Corticosteroid Derivatives
Prednisolone/Methylprednisolone is a semi-synthetic compound.
The mechanism Semi-synthetic corticosteroids prednisolone and methylprednisolone have altered structures that lessen the nephrotoxic adverse effects of natural corticosteroids. Nephrotic syndrome, glomerulonephritis, and autoimmune kidney disorders can all be effectively treated with these medications' strong anti-inflammatory and immunosuppressive properties.
Research: These corticosteroids lessen nephrotoxic damage in lupus nephritis and nephrotic syndrome and aid in the management of inflammatory kidney illnesses. [83–84]
5. Cisplatin Derivatives
Nedaplatin is a semi-synthetic platinum-based chemotherapeutic drug that has been chemically altered to lessen nephrotoxicity in comparison to cisplatin. It is utilized as a substitute for cisplatin in cancer treatment because of its better pharmacokinetic characteristics.
Research: Nedaplatin is a viable treatment option for cisplatin-induced nephrotoxicity, as evidenced by animal studies that indicate it produces reduced renal toxicity. [85–86]
6. Taxane Derivatives
Semi-Synthetic Substance: Paclitaxel/Docetaxel
Mechanism: Taxol, a naturally occurring substance obtained from the Pacific yew tree, is the semi-synthetic precursor to docetaxel and paclitaxel. These substances are used to treat a variety of malignancies as chemotherapy drugs. Compared to natural taxol, they are altered to increase stability, bioavailability, and efficacy while lowering nephrotoxic adverse effects.
Research: Studies indicate that paclitaxel and docetaxel are safer for long-term usage in the treatment of cancer and less nephrotoxic than their natural equivalents. [87–88]
7. Quinine Derivatives
Chloroquine/hydroxychloroquine is a semi-synthetic compound. Its mechanism These are altered forms of quinine, an alkaloid that is taken from the bark of the cinchona plant and used to treat malaria. In addition to being used to treat autoimmune disorders including rheumatoid arthritis and lupus nephritis, hydroxychloroquine and chloroquine have also been demonstrated to lessen nephrotoxicity in specific circumstances.
The semi-synthetic derivatives of quinine, chloroquine and hydroxychloroquine, have a safer profile with fewer kidney-related adverse effects, despite quinine's potential for nephrotoxicity. [89–90]
8. Herbal Derivatives
Semi-Synthetic Substance: Derivatives of Berberine
Mechanism: To improve its bioavailability and effectiveness in treating renal illnesses, berberine, an alkaloid obtained from a variety of plants, has undergone chemical modification. Its anti-inflammatory, anti-fibrotic, and antioxidant qualities help stop kidney damage and slow the course of chronic kidney disease (CKD).
Research: By lowering oxidative stress, fibrosis, and inflammation, berberine derivatives have been found to protect against diabetic nephropathy and induced nephrotoxicity. [91–92]
9. Flavonoid Derivatives
Semi-Synthetic Substance: Derivatives of Rutin and Quercetin
The mechanism Plant-derived flavonoids quercetin and rutin have undergone chemical modification to increase their kidney protective properties. These substances can lessen kidney damage brought on by nephrotoxic drugs like gentamicin and cisplatin because of their strong anti-inflammatory, anti-apoptotic, and antioxidant properties.
Research: Studies have shown that derivatives of rutin and quercetin have nephroprotective properties, enhancing kidney function in nephrotoxic situations. [93–94]
10. Glycoside Derivatives
Semi-Synthetic Substance: Digoxin and other cardiac glycosides
Mechanism: Heart failure and arrhythmias are treated with digoxin, a semi-synthetic derivative of the cardiac glycoside ouabain. By improving renal blood flow and lowering glomerular damage, it has demonstrated possible nephroprotective benefits in some mice, while being mostly utilized in cardiovascular treatment.
Research: Digoxin may enhance renal perfusion and function, particularly when heart failure is the cause of kidney injury. [95–96]
Synthetic Products for Nephrotoxicity
1. Angiotensin-Converting Enzyme (ACE) Inhibitors
For instance, Ramipril, Lisinopril, and Enalapril
Mechanism: Angiotensin I is converted to angiotensin II, a peptide that constricts blood vessels and encourages kidney injury, by ACE inhibitors. ACE inhibitors lower blood pressure, glomerular pressure, and proteinuria by blocking this route. These parameters are important in diabetic nephropathy and other types of chronic kidney disease (CKD).
Research: By enhancing renal function and lowering glomerular hypertension and glomerulosclerosis, ACE inhibitors have been demonstrated in studies to slow the course of kidney disease.
2. Angiotensin II Receptor Blockers (ARBs)
For instance, Irbesartan, Valsartan, and Losartan
Mechanism: Like ACE inhibitors, ARBs prevent angiotensin II from acting at its receptor location without interfering with the ACE enzyme. This helps prevent diabetic nephropathy, hypertensive nephropathy, and glomerulonephritis by lowering kidney vasoconstriction, salt retention, and fibrosis.
Research: Studies have shown that ARBs, especially in people with diabetes and hypertension, are useful in lowering proteinuria and slowing the course of CKD.
3. Statins
For instance, Rosuvastatin, Simvastatin, and Atorvastatin
Mechanism: The HMG-CoA reductase enzyme is inhibited by statins, which are medications that decrease cholesterol. Statins have been shown to have anti-inflammatory and antioxidant properties in addition to their ability to lower cholesterol. These properties may help shield the kidneys from harm caused by hyperlipidemia and diabetic nephropathy.
Research: Statins have been shown to lower proteinuria, maintain kidney function, and decrease the development of renal fibrosis and diabetic nephropathy.
4. Phosphodiesterase Type 5 (PDE5) Inhibitors
For instance, Vardenafil, Tadalafil, and Sildenafil
Mechanism: Although PDE5 inhibitors are mostly used to treat erectile dysfunction, they also increase renal blood flow through vasodilatory effects. By raising cyclic GMP levels, they can enhance glomerular filtration and lessen kidney damage brought on by diabetes and high blood pressure.
Research: PDE5 inhibitors are promising options for treating nephrotoxicity since preclinical and clinical trials have demonstrated that they may help lessen renal fibrosis, glomerular hypertension, and tubulointerstitial fibrosis.
5. Endothelin Receptor Antagonists
Bosentan and Ambrisentan, for instance
Mechanism: Endothelin-1, a strong vasoconstrictor that can result in renal fibrosis and glomerular damage, is inhibited by endothelin receptor antagonists. These medications can lower glomerular hypertension and stop the progression of renal fibrosis by inhibiting endothelin receptors.
Research: Preclinical and clinical research have indicated that these medications may help lessen kidney damage in diseases such as polyarteritis nodosa, diabetic nephropathy, and hypertensive nephropathy.
For instance, the mechanisms of sertraline, fluoxetine, and paroxetine have been demonstrated to have nephroprotective benefits by lowering oxidative stress, inflammation, and kidney tissue fibrosis, while being generally used for depression and anxiety.
Research: The potential of SSRIs to lessen tubulointerstitial fibrosis and diabetic nephropathy has been investigated. They could also assist CKD patients in reducing their proteinuria.
7. Metformin
Mechanism: A biguanide called metformin is used to treat type 2 diabetes. By increasing insulin sensitivity and reducing hepatic glucose synthesis, it lowers blood sugar levels. It has been demonstrated that metformin lowers the risk of diabetic nephropathy and increases glomerular filtration rate (GFR) in diabetic individuals.
Research: Metformin has demonstrated nephroprotective benefits when administered judiciously in individuals with early-stage diabetic nephropathy, despite concerns over the possibility of lactic acidosis in cases of severe renal impairment.
For instance, empagliflozin, dapagliflozin, and canagliflozin
Mechanism: SGLT2 inhibitors assist reduce blood glucose levels by blocking the kidneys' ability to reabsorb glucose. By lowering glomerular hyperfiltration, enhancing renal function, and lowering albuminuria, these medications also directly protect the kidneys.
Research: SGLT2 inhibitors have been shown in clinical trials to considerably slow the evolution of diabetic nephropathy, lower proteinuria, and postpone the need for dialysis in diabetic patients.
9. Corticosteroids (Synthetic)
For instance, methylprednisolone and prednisolone
Mechanism: Anti-inflammatory and immunosuppressive medications called synthetic corticosteroids are used to treat inflammatory kidney disorders and autoimmune illnesses. Particularly in diseases like glomerulonephritis, lupus nephritis, and nephrotic syndrome, they aid in lowering inflammation and immune-mediated kidney damage.
Research: Methylprednisolone and prednisolone work well to avoid kidney damage from autoimmune disorders and to treat inflammatory kidney illnesses.
10. Cilastatin
Mechanism: The synthetic drug cilastatin is used in conjunction with the broad-spectrum antibiotic imipenem. Cilastatin reduces imipenem's nephrotoxicity by blocking the renal enzyme dehydropeptidase-1, which stops imipenem from being broken down in the kidneys.
Research: When treating infections with imipenem, especially in individuals with renal impairment, cilastatin is utilized to avoid renal damage.
11. Carbapenem Derivatives
For instance, Ertapenem and Meropenem
Mechanism: Compared to more traditional antibiotics like gentamicin and amikacin, these synthetic broad-spectrum antibiotics have a lesser nephrotoxic profile because of their modified carbapenem structure.
Research: Studies have indicated that carbapenem derivatives, particularly meropenem, are less likely to cause nephrotoxicity and have a safer renal profile.
12. N-acetylcysteine (NAC)
Mechanism: Acetaminophen-induced liver damage is countered by NAC, a synthetic derivative of the amino acid cysteine. Because of its antioxidant qualities, NAC guards against oxidative stress, a major contributing factor to drug-induced nephrotoxicity.
Research: The nephroprotective properties of NAC are extensively investigated, especially in individuals receiving chemotherapy or gentamicin or other nephrotoxic medicines. [97–106]
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Abdel-Latif MA, Khalil RH. Assessment of hepatoprotective, nephroprotective efficacy, and oxidative stress responses to dietary Moringa oleifera leaf extract in Nile tilapia (Oreochromis niloticus) exposed to sub-chronic sodium fluoride. Food Sci Nutr. 2021;9(10):5584-5594.
Gupta P, Yadav DK, Siripurapu RK, Palit G, Maurya R. Nephroprotective role of alcoholic extract of Pterocarpus marsupium heartwood against experimentally induced diabetic nephropathy in rats. Pharm Biol. 2016;54(10):2243-2251. doi:10.3109/13880209.2016.1153665.
Kumar A, Nair V, Singh S, Gupta YK. Evaluation of anti-diabetic and anti-oxidative activity of Pterocarpus marsupium in experimental models. Indian J Clin Biochem. 2010;25(1):67-74.
Muthenna P, Akileshwari C, Reddy GB. Pterocarpus marsupium extract inhibits aldose reductase and advanced glycation end products in vitro: a possible therapy for diabetic complications. Phytother Res. 2012;26(7):1022-1027. doi:10.1002/ptr.3693.
Prescott LF, Illingworth RN, Critchley JA, et al. Intravenous N-acetylcysteine: the treatment of choice for paracetamol poisoning. BMJ. 1979;2(6198):1097-1100. doi:10.1136/bmj.2.6198.1097.
Liu Y, Liu JP, Xia Y. N-acetylcysteine for adults with acute kidney injury. Cochrane Database Syst Rev. 2020;2(2):CD007078.
Batist G, Barton J, Chaikin P, et al. Myocet (liposome-encapsulated doxorubicin citrate): a review of the pharmacology, pharmacokinetics, and clinical experience. Clin Breast Cancer. 2002;3(Suppl 2):S22-S28.
Gabizon A, Shmeeda H, Barenholz Y. Pharmacokinetics of pegylated liposomal Doxorubicin. Clin Pharmacokinet. 2003;42(5):419-436.
Kaye CM, Allen A, Poyser RH, et al. The clinical pharmacokinetics of amoxycillin. Clin Pharmacokinet. 1982;7(4):282-319.
Rodríguez-Baño J, Navarro MD, Retamar P, et al. β-lactam/β-lactam inhibitor combinations for serious infections caused by extended-spectrum β-lactamase-producing Enterobacteriaceae: a meta-analysis. Lancet Infect Dis. 2012;12(4):313-326.
Bolton WK, Remuzzi G, Heerspink HJL, et al. Effect of fostamatinib on kidney inflammation and fibrosis: Results from the fostamatinib for proteinuria due to diabetic nephropathy (FORTRESS) trial. Diabetes Care. 2020;43(10):2528-2535.
Bomback AS, Canetta PA, Beck LH, et al. Treatment of primary membranous nephropathy with rituximab: a systematic review. Clin J Am Soc Nephrol. 2009;4(4):734-744.
Arakawa T, Nakajima K, Iwashina M, et al. Comparative nephrotoxicity of cisplatin and nedaplatin in patients with head and neck cancer. J Int Med Res. 2020;48(5):300060520920464.
Yamamoto N, Nakagawa K, Nishimura Y, et al. Phase I study of nedaplatin and concurrent thoracic radiotherapy in patients with unresectable, locally advanced, non-small-cell lung cancer. J Clin Oncol. 2003;21(20):3835-3841.
Markman M. Liposomal formulations of anthracyclines: clinical utility in the treatment of cancer. Oncologist. 1999;4(2):87-92.
Rowinsky EK, Donehower RC. The clinical pharmacology of paclitaxel (Taxol). Semin Oncol. 1993;20(4 Suppl 3):16-25.
Schrezenmeier E, Dörner T. Mechanisms of action of hydroxychloroquine and chloroquine: implications for rheumatology. Nat Rev Rheumatol. 2020;16(3):155-166.
Mackenzie AH. Dose refinements in long-term therapy of rheumatoid arthritis with antimalarials. Am J Med. 1983;75(1A):40-45.
Zuo L, Zhou T, Pannell BK, et al. Berberine for kidney disease: A review of molecular mechanisms. Biomed Pharmacother. 2022;147:112671.
Li Z, Guo X, Huang X, et al. Protective effects of berberine on cisplatin-induced nephrotoxicity via anti-apoptotic and anti-inflammatory mechanisms in mice. Oncotarget. 2017;8(58):101567-101575.
Oteiza PI, Fraga CG, Galleano M. Quercetin and rutin as potential modifiers of oxidative stress in chronic diseases. Oxid Med Cell Longev. 2021;2021:6646921.
Boots AW, Haenen GR, Bast A. Health effects of quercetin: from antioxidant to nutraceutical. Eur J Pharmacol. 2008;585(2-3):325-337.
Hauptman PJ, Kelly RA. Digitalis. Circulation. 1999;99(9):1265-1270.
Gheorghiade M, Ferguson D. Digoxin: a neurohormonal modulator in heart failure? Circulation. 1991;84(5):2181-2186.
Lewis EJ, Hunsicker LG, Bain RP, Rohde RD. The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. N Engl J Med. 1993;329(20):1456-1462.
Brenner BM, Cooper ME, de Zeeuw D, et al. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med. 2001;345(12):861-869.
Tonelli M, Moye L, Sacks FM, Kiberd B, Curhan G. Pravastatin for secondary prevention of cardiovascular events in persons with mild chronic renal insufficiency. Ann Intern Med. 2003;138(2):98-104.
Wanner C, Inzucchi SE, Lachin JM, et al. Empagliflozin and progression of kidney disease in type 2 diabetes. N Engl J Med. 2016;375(4):323-334.
Tepel M, van der Giet M, Schwarzfeld C, Laufer U, Liermann D, Zidek W. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med. 2000;343(3):180-184.
Batist G, Gelmon KA, Chi KN, et al. Safety, pharmacokinetics, and efficacy of CPX-351 in patients with advanced solid tumors. Clin Cancer Res. 2015;21(4):985-992.
Himmelfarb J, Tuttle KR. New therapies for diabetic kidney disease. N Engl J Med. 2013;369(26):2549-2550.
Rauen T, Eitner F, Fitzner C, et al. Intensive supportive care plus immunosuppression in IgA nephropathy. N Engl J Med. 2015;373(23):2225-2236.
Ruggenenti P, Perna A, Remuzzi G. Retarding progression of chronic renal disease: the neglected promise of ACE inhibitors. BMJ. 2001;322(7277):368-372.
Pitt B, Bakris G, Ruilope LM, DiCarlo L, Mukherjee R. Serum potassium and clinical outcomes in the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS). Circulation. 2008;118(16):1643-1650.
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Gupta P, Yadav DK, Siripurapu RK, Palit G, Maurya R. Nephroprotective role of alcoholic extract of Pterocarpus marsupium heartwood against experimentally induced diabetic nephropathy in rats. Pharm Biol. 2016;54(10):2243-2251. doi:10.3109/13880209.2016.1153665.
Kumar A, Nair V, Singh S, Gupta YK. Evaluation of anti-diabetic and anti-oxidative activity of Pterocarpus marsupium in experimental models. Indian J Clin Biochem. 2010;25(1):67-74.
Muthenna P, Akileshwari C, Reddy GB. Pterocarpus marsupium extract inhibits aldose reductase and advanced glycation end products in vitro: a possible therapy for diabetic complications. Phytother Res. 2012;26(7):1022-1027. doi:10.1002/ptr.3693.
Prescott LF, Illingworth RN, Critchley JA, et al. Intravenous N-acetylcysteine: the treatment of choice for paracetamol poisoning. BMJ. 1979;2(6198):1097-1100. doi:10.1136/bmj.2.6198.1097.
Liu Y, Liu JP, Xia Y. N-acetylcysteine for adults with acute kidney injury. Cochrane Database Syst Rev. 2020;2(2):CD007078.
Batist G, Barton J, Chaikin P, et al. Myocet (liposome-encapsulated doxorubicin citrate): a review of the pharmacology, pharmacokinetics, and clinical experience. Clin Breast Cancer. 2002;3(Suppl 2):S22-S28.
Gabizon A, Shmeeda H, Barenholz Y. Pharmacokinetics of pegylated liposomal Doxorubicin. Clin Pharmacokinet. 2003;42(5):419-436.
Kaye CM, Allen A, Poyser RH, et al. The clinical pharmacokinetics of amoxycillin. Clin Pharmacokinet. 1982;7(4):282-319.
Rodríguez-Baño J, Navarro MD, Retamar P, et al. β-lactam/β-lactam inhibitor combinations for serious infections caused by extended-spectrum β-lactamase-producing Enterobacteriaceae: a meta-analysis. Lancet Infect Dis. 2012;12(4):313-326.
Bolton WK, Remuzzi G, Heerspink HJL, et al. Effect of fostamatinib on kidney inflammation and fibrosis: Results from the fostamatinib for proteinuria due to diabetic nephropathy (FORTRESS) trial. Diabetes Care. 2020;43(10):2528-2535.
Bomback AS, Canetta PA, Beck LH, et al. Treatment of primary membranous nephropathy with rituximab: a systematic review. Clin J Am Soc Nephrol. 2009;4(4):734-744.
Arakawa T, Nakajima K, Iwashina M, et al. Comparative nephrotoxicity of cisplatin and nedaplatin in patients with head and neck cancer. J Int Med Res. 2020;48(5):300060520920464.
Yamamoto N, Nakagawa K, Nishimura Y, et al. Phase I study of nedaplatin and concurrent thoracic radiotherapy in patients with unresectable, locally advanced, non-small-cell lung cancer. J Clin Oncol. 2003;21(20):3835-3841.
Markman M. Liposomal formulations of anthracyclines: clinical utility in the treatment of cancer. Oncologist. 1999;4(2):87-92.
Rowinsky EK, Donehower RC. The clinical pharmacology of paclitaxel (Taxol). Semin Oncol. 1993;20(4 Suppl 3):16-25.
Schrezenmeier E, Dörner T. Mechanisms of action of hydroxychloroquine and chloroquine: implications for rheumatology. Nat Rev Rheumatol. 2020;16(3):155-166.
Mackenzie AH. Dose refinements in long-term therapy of rheumatoid arthritis with antimalarials. Am J Med. 1983;75(1A):40-45.
Zuo L, Zhou T, Pannell BK, et al. Berberine for kidney disease: A review of molecular mechanisms. Biomed Pharmacother. 2022;147:112671.
Li Z, Guo X, Huang X, et al. Protective effects of berberine on cisplatin-induced nephrotoxicity via anti-apoptotic and anti-inflammatory mechanisms in mice. Oncotarget. 2017;8(58):101567-101575.
Oteiza PI, Fraga CG, Galleano M. Quercetin and rutin as potential modifiers of oxidative stress in chronic diseases. Oxid Med Cell Longev. 2021;2021:6646921.
Boots AW, Haenen GR, Bast A. Health effects of quercetin: from antioxidant to nutraceutical. Eur J Pharmacol. 2008;585(2-3):325-337.
Hauptman PJ, Kelly RA. Digitalis. Circulation. 1999;99(9):1265-1270.
Gheorghiade M, Ferguson D. Digoxin: a neurohormonal modulator in heart failure? Circulation. 1991;84(5):2181-2186.
Lewis EJ, Hunsicker LG, Bain RP, Rohde RD. The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. N Engl J Med. 1993;329(20):1456-1462.
Brenner BM, Cooper ME, de Zeeuw D, et al. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med. 2001;345(12):861-869.
Tonelli M, Moye L, Sacks FM, Kiberd B, Curhan G. Pravastatin for secondary prevention of cardiovascular events in persons with mild chronic renal insufficiency. Ann Intern Med. 2003;138(2):98-104.
Wanner C, Inzucchi SE, Lachin JM, et al. Empagliflozin and progression of kidney disease in type 2 diabetes. N Engl J Med. 2016;375(4):323-334.
Tepel M, van der Giet M, Schwarzfeld C, Laufer U, Liermann D, Zidek W. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med. 2000;343(3):180-184.
Batist G, Gelmon KA, Chi KN, et al. Safety, pharmacokinetics, and efficacy of CPX-351 in patients with advanced solid tumors. Clin Cancer Res. 2015;21(4):985-992.
Himmelfarb J, Tuttle KR. New therapies for diabetic kidney disease. N Engl J Med. 2013;369(26):2549-2550.
Rauen T, Eitner F, Fitzner C, et al. Intensive supportive care plus immunosuppression in IgA nephropathy. N Engl J Med. 2015;373(23):2225-2236.
Ruggenenti P, Perna A, Remuzzi G. Retarding progression of chronic renal disease: the neglected promise of ACE inhibitors. BMJ. 2001;322(7277):368-372.
Pitt B, Bakris G, Ruilope LM, DiCarlo L, Mukherjee R. Serum potassium and clinical outcomes in the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS). Circulation. 2008;118(16):1643-1650.
Naveen Tripathi
Corresponding author
Department of Pharmacy, Institute of Technology and Management, GIDA, Gorakhpur, Uttar Pradesh, India, 273209
10.5281/zenodo.15528332
