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American Journal of  
Chemistry and Pharmacy (AJCP)

Oral Acyclovir Induced Acute Kidney Injury
Yasser Sadawey1*, Yasameen Abdulhameed1

Volume 1 Issue 2, Year 2022
ISSN: 2834-0116 (Online)

DOI: https://doi.org/10.54536/ajcp.v1i2.829
https://journals.e-palli.com/home/index.php/ajcp

Article Information ABSTRACT

Received: October 18, 2022

Accepted: October 29, 2022

Published: November 01, 2022

Acyclovir is an antiviral medication often used to treat outbreaks of  herpes in children. 
Acyclovir has an exceptional safety profile; there is a possibility that it might induce severe 
nephrotoxicity in rare cases. In this report, we present the case of  a 17-year-old girl with 
acute renal injury as a side effect of  using acyclovir. The patient was admitted for three days 
due to drug-induced AKI, which was reversed by discontinuing the afflicted medicine (acy-
clovir), initiating appropriate hydration with intravenous normal saline 0.9%, and refraining 
from any nephrotoxic medications. Following up a week later, the patient was asymptomatic 
and had normal kidney function. Therefore, it is critical to use acyclovir correctly to avoid 
possibly fatal consequences.

Keywords
Oral Acyclovir, Acute Kidney 
Injury, Acyclovir Nephrotoxicity, 
Medicine

1 Department of  Medicine, Mediclinic ME, Al Jowhara Hospital, AL Ain, UAE
* Corresponding author’s e-mail: yassersadawey12@outlook.com

INTRODUCTION
Acyclovir is now the most effective treatment for several 
herpes viruses, such as herpes encephalitis (Balfour H. 
H., 1984; YY., 1984), varicella zoster virus (VZV), or 
herpes simplex virus (HSV) infections in children with 
compromised immune systems. In addition, high-dose 
intravenous acyclovir to combat viral infections may be 
beneficial (YY., 1984). The adverse effects of  acyclovir are 
well-known; nonetheless, most people do not consider it. 
The most prevalent underlying mechanism that acyclovir 
may generate is crystal nephropathy, which is reported 
to have the adverse side effect of  inducing acute renal 
injury (AKI). It is hypothesized that the mechanism that 
causes the damage is the precipitation and crystallisation 
of  the medicine inside the renal tubules, which results in 
obstruction and perhaps cellular necrosis (Izzedine, 2005; 
Mason, 2008). Patients with acyclovir-induced acute 
kidney injury have a fast reduction in their renal function 
and an increase in their blood creatinine level. This usually 
occurs between 12 and 48 hours after administering the 
medicine (Yildiz C, 2013; Zhang Y, 2016). Appropriate 
diagnosis and management of  AKI caused by acyclovir 
are necessary for an effective prognosis(Zhang Y, 2016). 
In this report, we present a case of  a 17-year-old girl 
who developed an acute kidney injury as a side effect of  
acyclovir in the management of  herpes zoster infection.

METHODOLOGY
Case Presentation
Seventeen years old female with known epilepsy was 
admitted to our hospital. She was diagnosed five years ago 
with epilepsy and started on treatment for a few weeks 
with poor compliance due to medication side effects. She 
has a five-day history of  skin rash affecting her upper 
back and right shoulder (itchy, vesicular, painful, and 

affecting a dermatomal distribution of  cervical 4,5 and 
6) associated with nausea and vomiting at the time of  
admittance in another facility. During that period, she 
was started on acyclovir 800 mg orally three times daily 
for the diagnosis of  herpes zoster infection, Diclofenac 
sodium 50 mg twice and levetiracetam 500 mg orally 
every 12 hours. Unfortunately, she was discharged one 
day before her current presentation to our hospital. She 
also gave a history of  reduced urine output. Upon arrival, 
she was vitally stable and afebrile, weighted 60 kg with 
normal capillary refill time but dry mucous membranes. 
Systemic examination, apart from mild epigastric 
tenderness, was reported as unremarkable. Neurological 
examination revealed unremarkable results, including 
motor, sensory, cranial nerves, and cerebellar functions, 
and no photophobia or neck stiffness.
Chest X-ray and ultrasound abdomen were unremarkable. 
CT head done earlier showed mucosal thickening and 
retention cyst of  left maxillary sinuses. Her laboratory 
results showed creatinine of  202wµ mol/L, normal 
electrolytes and pH 7.33, and HcO3 18 mEq/L, lactate 
0.8 mmol/L. She was admitted as having acute kidney 
injury, probably drug-induced, using the Naranjo 
algorithm of  adverse drug reaction. The patient was 
admitted for three days as drug-induced AKI, and the 
culprit drug (acyclovir) was stopped with the initiation 
of  proper hydration with normal intravenous saline 
0.9% and avoiding all nephrotoxic medications. She was 
started on metoclopramide 10 mg intravenous when 
needed, pantoprazole 40 mg intravenous once daily, and 
paracetamol 1 gm for pain control, daily renal function 
tests showed improvement of  kidney functions, and 
she was tolerant of  oral intake. Upon follow-up a week 
later, a patient had normal kidney functions and was 
asymptomatic.

https://doi.org/10.54536/ajcp.v1i2.829
https://journals.e-palli.com/home/index.php/ajcp
mailto:yassersadawey12%40outlook.com?subject=


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Table 1: Laboratory Values of admitted case
Normal Value Feb 2021 

Baseline
2 days pre 
admission

1 day pre 
admission

Day 1
Admission

Day 2 Day 3 Follow 
up in 1 
week

Sodium 136-145 mmol/L 140 139 139 138 141 140 136
Potassium 3.2-5.5 mmol/L 4.3 4.2 4.2 4.2 3.8  4.5
Chloride 98-107 mmol/L 105 104 103 101.4 106.6 103.8  
Urea 2.8-8.1 mmol/L 6.3 4.5 6.5 9.1 6.9 3.9 3.7
Creatinine 34-80 micrmol/L 56 118 231 206 148 82 65
CO3 22-29 mmol/L 26 24 19  -  -  -  -
pH 7.35-7.45 NA 7.35 7.35  -  -  -  -
CRP <5mg/L NA 5.3 28.8 35 26 10  -
Alkaline 
Phosphatase

48-95 U/L  -  -  - 109  -  -  -

ALT 0-17 U/L  -  -  - 12.2  - 11.1  -
Amylase 29-118 U/L  -  -  - 57  -   -
AST 0-23 U/L  -  -  - 15.8  - 13  -
Calcium 2.31-2.64 mmol/L  -  -  - 2.35  -  -  -
TSH 0.5-4.5 mi-

croIU/ml
 -  -  -  -  - 1.89  -

HCT (PCV) 31-42%  -  -  - 32.8  - 29.4 34.9
Haemoglobin 10.9-14.3 g/dL  -  -  - 10.6  - 9.5 11.2
Basophils % 0.4-1.3%  -  -  - 0.3  - 0.4 0.5
Eosinophils % 0.4-8.2 %  -  -  - 1.2  - 2.4 3.1
Lymphocytes % 20.1-48.8 %  -  -  - 27.6  - 28.8 5.7
MCH 24.7-32.8 pg  -  -  - 23  - 22.9 23.2
MCHC 32.3-35.6g/dL  -  -  - 32.3  - 32.4 32
MCV 75.5-95.3 fL  -  -  - 71.3  - 70.7 72.4
Monocytes % 4.10-12.90%  -  -  - 11.3  - 13 10.3
Neutrophils % 42.8-75.1 %  -  -  - 59.6  - 55.4 80.4
Platelet count 150-410  10³/ųL  -  -  - 249  - 237 264
Red Cell Count 3.63-4.92  10⁶/ųL  -  -  - 4.6  - 4.15 4.82
White Cell 
Count

3.8-11.8  10⁶/ųL  -  -  - 6.7  - 6.2 7.4

Urine Rotine  -  -  -  -  -  -  -  -
Blood (RBC) negative  -  -  - Negative  - Negative  -
Ketone negative  -  -  - Positive +  - Negative  -
Protein negative  -  -  - Negative  - 10 mg/dl  -
Amorphous 
Urate

Nil  -  -  - Nil  - Nil  -

Amorphous 
Phosphate

Nil  -  -  - Nil  - Nil  -

Bilirubin negative  -  -  - Negative  - Negative  -
Crystals Nil  -  -  - Nil  - Nil  -
Fatty casts Nil  -  -  - Nil  - Nil -
Granular Casts Nil  -  -  - Nil  - Nil  -
Hyaline Casts Nil  -  -  - Nil  - Nil  -



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RBC casts Nil  -  -  - Nil  - Nil  -
WBC casts Nil  -  -  - Nil  - Nil  -
Glucose negative  -  -  - Negative  - Negative  -
Leukocytes 0-5  cell/HPF  -  -  - 10-Jun  - 0-5  -
Leukocyte 
esterase 

negative  -  -  - Positive +  - Negative  -

Nitrite negative  -  -  - Negative  - Negative  -
pH 5-9  pH  -  -  - 5  - 6  -
Bacteria Nil  -  -  - Few ++  - Nil  -
Specific 
Gravity

1.003 - 1.035  -  -  - 1.01  - 1.009  -

DISCUSSION
Nephropathy caused by oral acyclovir is uncommon and 
only manifests itself  at very high doses (more than 500 
mg/m2) when the medication is used by patients whose 
volume status has significantly reduced (Perazella., 1999). 
It is critical to know the possible nephrotoxicity for the 
patients being treated with acyclovir. Our patient had an 
acute kidney injury while taking oral acyclovir and other 
nephrotoxic drugs and being volume depleted, but her 
creatinine improved when acyclovir stopped Therefore, 
acyclovir crystalluria and subsequent intrarenal 
obstruction and nephropathy would be the most 
plausible explanation for the observed renal injury, even 
if  the crystals were undetected on regular urine analysis. 
In individuals with underlying volume depletion and 
renal insufficiency, acyclovir dosage should be lowered. 
To avoid crystallisation and eventual tubular blockage, 
gradual medication infusion over 1-2 hours, appropriate 
fluid replenishment, and introduction of  high urine flow 
rates (100-150 ml/h) should be recommended (Brigden et 
al., 1982; Sawyer et al., 1988).
Renal function should be monitored regularly in patients 
receiving high-dose intravenous acyclovir in patients 
diagnosed with renal impairment at any dosage level. 
Common symptoms include unusual sickness, nausea, 
abdominal discomfort, vomiting, and muscle twitching 
while receiving treatment (Wade JC, 1983). 
When serum creatinine levels rise, acyclovir must 
be managed to be discontinued. Hydration should 
be maintained during therapy to ensure a high urine 
flow(Gunness P, 2010). If  no improvement is observed 
in patients with renal function soon after discontinuing 
acyclovir, other causes of  renal toxicity should be 
sought. Treatment may be maintained at a lower dose 
for secondary infections that respond to acyclovir while 
a renal function is closely monitored. Since volume 
contraction may go undiagnosed in outpatients treated 
with  acyclovir, they are more susceptible to acyclovir-
induced kidney damage(Chawla, 2017). 

CONCLUSION
It is concluded that to prevent morbidity, acute kidney 
injury must be diagnosed as soon as possible (Ratan., 

2003). Since acyclovir is frequently prescribed for renal 
transplantation, patients with herpes simplex virus and 
herpes zoster infections, and patients with Neurological 
viral infections, therefore, practitioners must be aware 
of  the associated risk, side effects, and how drug-related 
issues might be addressed.

Ethical Approval
Ethical approval for this study was obtained from 
Mediclinic Al Jowhara Hospital (Reference number: 
UHN: 1238416). All procedures performed in the study 
involving the patient were by the ethical standards of  
the governmental guidelines and with the 1964 Helsinki 
Declaration and its later amendments or comparable 
ethical standards.

Conflict of  Interest
The authors declare that there is no conflict of  interest 
regarding the publication of  this case report.

Funding
Any grants did not fund this work.

Informed Consent 
Written informed consent was obtained from the 
participant.

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Brigden, D., Rosling, A. E., & Woods, N. C. (1982). Renal 
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Chawla, L., Bellomo, R., Bihorac, A. et al. . (2017). Acute 
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