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Kidney failure is an irreversible progressive malfunction which often develops into chronic kidney disease (CKD) and end-stage renal disease (ESRD). The spectrum of CKD varies from proteinuria to elevated creatinine and ESRD. This case report describes a 60-year-old man, who despite being at the stage four of CKD for 4 years, had a case history of amelioration of renal function upon watermelon consumption.
Regression of kidney malfunction upon watermelon
Amin Hasanvand1, Reza Mohammadrezaei Khorramabadi2, Mohammad Reza Tamadon3*
1Department of Pharmacology and toxicology, Faculty of Pharmacy, Lorestan University of Medical Sciences, Khorramabad, Iran
2Student Research Committee, Lorestan University of Medical Sciences, Khorramabad, Iran
3Department of Internal Medicine, Semnan University of Medical Sciences, Semnan, Iran
Copyright © 2018 The Author(s);Published by Society of Diabetic Nephropathy Prevention. This is an open-access article distributed under
the terms of the Creative Commons Attribution License (, which permits unrestricted use,
distribution, and reproduction in any medium, provided the original work is properly cited.
Chronic kidney malfunction is an
irreversible progressive process, which
often leads to chronic kidney disease (CKD)
and end-stage renal disease (ESRD). Its
chief causes include diabetes, high blood
pressure, secondary glomerulonephritis
(GN), conventional cystic diseases,
interstitial nephritis, chronic pyelonephritis,
secondary GN and vasculitis. Chronic renal
failure (CRF) is defined as the irreversible
progressive decline in kidney functionality.
This progressive failure is represented by a
gradual increase in plasma creatinine along
with a decrease in glomerular filtration rate.
The aim of treatment is to apply an alternative
treatment using dialysis or kidney transplant
before uremia symptoms appear (1).
Stages of CRF include decrease in kidney
functionality, kidney failure and ESRD.
The intensity of the decline in kidney
functionality and presence of CRF depend
on underlying dysfunction, proportion of
proteinuria and existence or non-existence
of hypertension. In patients who had
proteinuria or hypertension, the disease
progression was faster (2,3).
CKD consists of five stages. Stage one is
related to kidney damage with near normal
glomerular filtration rate (GFR) (90 cc/min).
At the first stage of kidney disease, the aim of
treatment is to slow down the pace of CKD
and to reduce the risk of heart and coronary
diseases. Stage two concerns kidney damage
with a minor decrease in GFR (between
60 and 89 cc/min). An assessment on the
progression of CKD is a key point in the
diagnosis and treatment of the disease.
Additionally, modalities require to slow the
reduction process of glomerular damage
are also crucial. Stage three refers to the
decrease in the average of GFR (between 30
and 59 cc/min). When a CKD reaches this
point, disorders such as anemia and bone
complications should be examined. Stage
four is related to a significant reduction
in GFR (between 15 and 29 cc/min), and
finally stage five, which is the last stage of
kidney disease (GFR lower than 15 cc/min),
requires dialysis or kidney transplant (4).
It is recommended for CKD patients to
follow a healthy diet. However, there is no
consensus on the type of foods. Generally,
low-protein diets as well as low-salt diets
*Correspondence to
Mohammad Reza
Tamadon, E-mail: mrt_
Received 10 October 2017
Accepted 8 December 2017
ePublished 5 January 2018
Keywords: Chronic kidney
disease, Renal disease,
Citation: Hasanvand
A, Mohammadrezaei
Khorramabadi R,
Tamadon MR.
Regression of
kidney malfunction
upon watermelon
Ann Res Antioxid.
Kidney failure is an irreversible progressive malfunction which often develops into chronic kidney
disease (CKD) and end-stage renal disease (ESRD). The spectrum of CKD varies from proteinuria to
elevated creatinine and ESRD. This case report describes a 60-year-old man, who despite being at the
stage four of CKD for 4 years, had a case history of amelioration of renal function upon watermelon
Ann Res Antioxid. 2018;3(1):e07 Case Report
Annals of Research in Antioxidants http
Core tip
Chronic kidney malfunction is an irreversible
progressive process, which often leads to
chronic kidney disease (CKD) and end-stage
renal disease (ESRD). Stages of CRF include
decrease in kidney functionality, kidney
failure and ESRD. The intensity of the decline
in kidney functionality and presence of CRF
depend on underlying dysfunction, proportion
of proteinuria and existence or non-existence
of hypertension.
Hasanvand A et al
Annals of Research in Antioxidants 2Volume 3, Issue 1, January 2018
are recommended. Nevertheless, such diets may even
increase mortality and morbidity due to malnutrition (5).
In this case report, we present a male patient with CKD,
who was able to reach a stable state following watermelon
Case Report
The patient is a 60-year-old man with symptoms of kidney
disease, who has regularly visited by his physician for five
years. The patients laboratory results on the primary
visit were as follows: serum BUN=75 mg/dL, serum
creatinine = 9.6 mg/dL and blood pressure was 120/80
mm Hg. The patient was a diabetic since the age of 30.
The patient was examined, and then started to receive
conventional treatments. He was recommended to visit
the doctor regularly. In next visits, his blood pressure
was 120/80 mm Hg. His creatinine level rose from 2 to
9.6 mg/dL and his BUN level drastically increased from
27 to 48 mg/dL, when he was operated for his colonic
cancer. Since he was a diabetic, the patient received the
conventional treatments for diabetes. He stated that he
consumed a significant amount of watermelon on a daily
regimen, without changing the drugs. Meanwhile, serum
creatinine regressed to 1.7 mg/dL.
The universal prevalence of CKD has been reported to be
between 8% and 16% (6,7). Its prevalence rates by country
are; 9.3% in Norway, 11% in the US, 16% in Australia,
9.07% in Malaysia and 13.5% in England (5,6). CKD
prevalence has been studied at different stages by Coresh
et al. According to that study, 3.3% were at stage one, 3%
were at stage two, 0.75% were at stage three, 0.2% were at
stage four and 0.2% were at stage five. In their study, age
has been described as a key predictor of CKD, as 11% of the
people older than 65 who were not suffering high blood
pressure or diabetes were at stage three or higher stages
(8). CKD is a progressing disease. The patients at stage
one will show symptoms of kidney damage despite having
a GFR near 90 cc/min. At stage three, the symptoms start
to develop and at stage four they experience a significant
decrease in their GFR levels. At stage five, GFR drops to
a level lower than 15 cc/min and the patient will need to
kidney transplant or dialysis (8).
The common hypothesis is that the patient suffering
CKD will also suffer from progressing nephropathy
with varying paces of advancement. Proteinuria and
hypertension, are key factors for the pace of development
being increased (9). Most of the people suffering from
CKD experience a progressing decrease in their kidney
functionality. However, some of clinical trials show
that some patients had sustained kidney functionality
during the follow-ups (10). There was no similar case
in the relevant scientific literature. In some sources,
there are some points about the benefits of watermelon
consumption for kidney patients. For instance, in one
source it has been recommended that patients suffering
CKD at various stages should benefit from watermelon
consumption except in terminal phage of renal function,
while there is the risk of hyperkalemia (11). In another
source it has been claimed that consuming watermelon
in the early stages of CKD is permitted and can be even
of help due to its diuretic characteristic. In any case, since
these patients have special conditions, nutrition should
not be dismissed (12).
In another source, patients suffering hyperkalemia
and those at stage three or higher of CKD have been
urged not to consume watermelon (13). In most of the
reviewed resources, the benefits of watermelon have been
mentioned but in no resource there has been any reference
to its effect on the reduction of blood urea and creatinine
of CKD patients. These foretold benefits of watermelon
are due to its compounds. Watermelon contains an
important anti-oxidant called lycopene which is useful in
improving prostate cancer. Some studies have indicated
that the consumption of lycopene prevents kidney
damages due to its biochemical and histopathological
parameters (8,14). Citrulline and arginine are some of the
other compounds existed in watermelon. They contribute
to a healthy blood flow. In some sources it has been stated
that adding compliments containing arginine to the
diet is helpful especially for kidney failure patients. This
modality may have a potential effect on treating kidney
diseases by stopping biochemical processes that produce
non-nitric oxide (which reduces the asymmetric activity
of dimethylarginine) (15-23).Watermelon is a nutrient
full of anti-oxidants. The effects of anti-oxidants in
preventing different diseases and their progression have
been confirmed in various studies (19,24).
Therefore, it can be claimed that a reduction in BUN
and creatinine level has occurred in our patient after
consuming a significant amount of watermelon and the
consequent increase in anti-oxidants level in his blood
as well as the subsequent effect of these compounds on
kidney function. The disease has not further developed
despite high urea and creatinine level in the patient’s
blood. Furthermore, these parameters have decreased
gradually over the years. He has now a BUN level of 24
mg/dL and creatinine level of 1.5 mg/dL. There also has
been a significant rise in these parameters whenever he
stopped consuming watermelon and a decrease back to
the previous levels whenever he resumed watermelon
Authors’ contribution
All authors contributed to the manuscript equally. MRT managed
and handled the patient. RM and AH prepared the primary draft.
MRT edited and finalized the manuscript. All authors read and
signed the final paper.
Conflicts of interest
The authors declared no competing interests.
Ethical considerations
Ethical issues (including plagiarism, data fabrication, double
publication) have been completely observed by the authors. The
Kidney and watermelon
Annals of Research in Antioxidants 3Volume 3, Issue 1, January 2018
patient gave his consent for publication this case report.
1. Nesrallah GE, Mustafa RA, Clark WF, Bass A, Barnieh L,
Hemmelgarn BR, et al. Canadian Society of Nephrology 2014
clinical practice guideline for timing the initiation of chronic
dialysis. CMAJ. 2014;186:112-7. doi: 10.1503/cmaj.130363.
2. Tamadon MR. Secondary hyperparathyroidism and chronic
kidney disease. J Parathyr Dis. 2013;1:15–6
3. Abboud H, Henrich WL. Clinical practice. Stage IV chronic
kidney disease. N Engl J Med. 2010;362:56-65. doi: 10.1056/
4. Levey AS, de Jong PE, Coresh J, El Nahas M, Astor BC,
Matsushita K, et al. The definition, classification, and
prognosis of chronic kidney disease: a KDIGO Controversies
Conference report. Kidney Int. 2011;80:17-28. doi: 10.1038/
5. Martin WF, Armstrong LE, Rodriguez NR. Dietary protein
intake and renal function. Nutr Metab (Lond). 2005;2:25. doi:
6. Gheissari A, Hemmatzadeh S, Merrikhi A, Fadaei Tehrani
S, Madihi Y. Chronic kidney disease in children: A report
from a tertiary care center over 11 years. J Nephropathol.
2012;1:177-82. doi: 10.5812/nephropathol.8119.
7. Jha V, Garcia-Garcia G, Iseki K, Li Z, Naicker S, Plattner
B, et al. Chronic kidney disease: global dimension and
perspectives. Lancet. 2013;382:260-72. doi: 10.1016/S0140-
8. Coresh J, Astor BC, Greene T, Eknoyan G, Levey AS. Prevalence
of chronic kidney disease and decreased kidney function in
the adult US population: Third National Health and Nutrition
Examination Survey. Am J Kidney Dis. 2003;41:1-12. doi:
9. Mardani S, Nasri P, Tavakoli M. Contrast induced nephropathy;
recent findings. J Nephropharmacol. 2013;2:27-30.
10. Fogo AB. Progression and potential regression of
glomerulosclerosis. Kidney Int. 2001;59:804-19. doi:
11. Can Stage 3 Kidney Failure Patients Eat Watermelon. http://
12. Is Watermelon Good to Lower Creatinine 2012. http://www.
13. Is Watermelon Good for Stage 3 CKD Patients 2012. http://
14. Amiri M, Nasri H. Secondary Hyperparathyroidism in chronic
kidney disease patients; current knowledge. J Parathyr Dis.
15. Rimando AM, Perkins-Veazie PM. Determination of citrulline
in watermelon rind. J Chromatogr A. 2005;1078:196-200.
16. Collins JK, Wu G, Perkins-Veazie P, Spears K, Claypool PL,
Baker RA, et al. Watermelon consumption increases plasma
arginine concentrations in adults. Nutrition. 2007;23:261-6.
doi: 10.1016/j.nut.2007.01.005.
17. Cherla G, Jaimes EA. Role of L-arginine in the pathogenesis
and treatment of renal disease. J Nutr. 2004;134:2801S-2806S.
18. Baylis C. Arginine, arginine analogs and nitric oxide
production in chronic kidney disease. Nat Clin Pract Nephrol.
2006;2:209-20. doi: 10.1038/ncpneph0143.
19. Martens CR, Edwards DG. Peripheral vascular dysfunction in
chronic kidney disease. Cardiol Res Pract. 2011;2011:267257.
doi: 10.4061/2011/267257.
20. Lau T, Owen W, Yu YM, Noviski N, Lyons J, Zurakowski D, et
al. Arginine, citrulline, and nitric oxide metabolism in end-
stage renal disease patients. J Clin Invest. 2000;105:1217-25.
21. Chen GF, Baylis C. In vivo renal arginine release is impaired
throughout development of chronic kidney disease. Am J
Physiol Renal Physiol. 2010;298:F95-102. doi: 10.1152/
22. Chiang SS, Tai CW, Chung CJ, Shiue HS, Chen JB, Su CT, et al.
Micronutrients and lifestyles in Taiwanese patients with stage
3 to 5 chronic kidney disease. Nutrition. 2010;26:276-82.
doi: 10.1016/j.nut.2009.04.021.
23. Kachhawa K, Varma M, Kachhawa P, Agrawal D, Shaikh M,
Kumar S. Study of dyslipidemia and antioxidant status in
chronic kidney disease patients at a hospital in South East
Asia. J Health Res Rev. 2016;3:28-30.
24. Pierine DT, Navarro ME, Minatel IO, Luvizotto RA,
Nascimento AF, Ferreira AL, et al. Lycopene supplementation
reduces TNF-alpha via RAGE in the kidney of obese rats. Nutr
Diabetes. 2014;4:e142. doi: 10.1038/nutd.2014.39.
ResearchGate has not been able to resolve any citations for this publication.
Full-text available
Contrast induced nephropathy is one cause of acute renal failure. Contrast induced nephropathy is the third most common cause of hospital-acquired acute renal failure. The incidence of contrast induced nephropathy in the general population is 0.6% to 2.3%, but when focusing on specific high-risk patients the incidence can increase to more than 40%. Studies suggest that intravenous hydration is the most effective strategy to prevent contrast induced nephropathy. Hydration is inexpensive and is usually risk-free. Administration of optimal fluids before and after the contrast procedure allows for increased urine output and improved outcomes.
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A 54-year-old woman with an 11-year history of type 2 diabetes presents for care. She was first noted to have proteinuria 4 years earlier; her serum creatinine level then was 1.1 mg per deciliter (97 mu mol per liter). Her urinary protein excretion has progressively increased to 2.8 g per 24 hours, and her serum creatinine level to 3.1 mg per deciliter (274 mu mol per liter). The estimated glomerular filtration rate (GFR) is 26 ml per minute per 1.73 m(2) of body-surface area. Her blood pressure is 155/90 mm Hg, and the glycated hemoglobin level is 7.6 mg per deciliter. The medications she is currently taking include an oral hypoglycemic agent, an angiotensin-converting-enzyme (ACE) inhibitor, a statin, and a thiazide diuretic. How should her case be managed?