The Official Journal of the College of Medicine, Ekiti State University; Ekiti State University Teaching Hospital, and

the Medical and Dental Consultants

Association of Nigeria (MDCAN) EKSUTH Branch
www.nigerianstethoscope.org e-ISSN: 2714-4305 p-ISSN: 2714-3635

Nephrolithiasis-Induced Chronic Kidney Disease – a Case Report

Olanrewaju TO1, Busari KA1, Oyedepo DS1, Adeyemo AW1

1
Division of Nephrology, Department of Medicine, University of Ilorin and University of Ilorin Teaching
Hospital, Ilorin, Kwara State, Nigeria
Corresponding Author’s E-mail: olanrewaju.to@umilorin.edu.ng; timothy.o.olanrewaju@gmail.com

Received: October 2, 2022

Accepted for publication: November 11, 2022
Published online: December 30, 2022
_______________________________________________________________________________________________________________

Abstract
A 35-year old woman presented with recurrent bilateral flank pain of 9 years duration. The current episode
started 10 days earlier, and it was associated with profound lethargy, recurrent vomiting and fever. She
was referred from a private hospital where she has had two units of blood. She had used antibiotics and
herbal remedies repeatedly since onset of the illness. Examination revealed a chronically ill looking
woman who was pale, afebrile, had bilateral renal angle tenderness. Investigations revealed anaemia,
leukocytosis, azotaemia and evidence of bilateral nephrolithiasis and moderate hydronephrosis on imaging
studies. An assessment of bilateral pyelonephritis on background chronic kidney disease (CKD) secondary
to obstructive nephropathy from nephrolithiasis was made. She was treated with parenteral antibiotics,
liberal fluid therapy and counselled for surgical intervention.
This case highlights an uncommon case of bilateral nephrolithiasis and the link between nephrolithiasis
and chronic kidney disease as well as the impact early presentation and management may have in
preventing this complication.

Keywords: Nephrolithiasis, Chronic kidney disease, Hydronephrosis, Obstructive nephropathy, Pyelonephritis.

improvement. The previous ultrasound scan done

1. Introduction
Case Presentation
Mrs. A.M. is a 35-year old hair-dresser who
presented with a 9 year history of recurrent bilateral
flank pain. The flank pain was worse on the right,
dull-ache, sometimes colicky, and radiating to the
back and groin. It was severe that it prevents sleep
and limits daily activities, but temporarily relieved
by analgesics. The pain lasts for a few days at a time
with pain-free periods lasting weeks to months. She
had been treated repeatedly at patent medicine
stores and private hospitals without significant
1
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revealed bilateral kidney stones. The current
episode started 10 days before presentation, with
severe right-sided dull-ache loin pains, which was
continuous, but non-radiating. There was no
associated suprapubic pain, haematuria, passage of
stones per urethra, dysuria, urinary frequency or
reduction in urine output. However, there was
associated recurrent vomiting, hiccups and
progressive malaise. She had fever which was high
grade, intermittent and associated with chills and
rigors. She does not consume a high meat or dairy
products. She had presented to a private hospital
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where she had intravenous antibiotics, fluids, and
was transfused with 2 units of blood for the first
time, The pre-transfusion packed cell volume was
not known. She is not a previously known
hypertensive or diabetic. Her genotype is AA. She
had no history suggestive of underlying
malignancy. There was no family history of kidney
stones, chronic kidney disease (CKD), hypertension
or diabetes. She does not smoke cigarettes nor
consumes alcoholic beverages.
On general physical examination, she was
chronically ill looking, pale, anicteric, afebrile with
an axillary temperature of 370C, not dehydrated and
she had no pedal oedema. Abdominal examination
revealed a full abdomen that was soft, moved with
respiration, and marked right-sided renal angle
tenderness. The kidneys were not bimanually
palpable and no organomegaly or ascites. She had a
pulse rate of 106 beats per minute, regular, good
volume, a blood pressure of 110/80mmHg, no other
abnormality noted on precordial examination.
There were no abnormalities detected on the
respiratory or nervous system examinations. An
initial assessment of right sided pyelonephritis on a
background of nephrolithiasis, to rule out
obstructive nephropathy was made.
Investigations: The results of the investigations are
shown in Tables 1, and 2; and below.

Table 1: Serial serum electrolytes, urea and creatinine

Date Sodium Potassium Urea Creatinine Calcium Phosphate Urate eGFR

mmol/l mmol/l mmol/l µmol/l mmol/l mmol/l mmol/l ml/min

At 132 7.0 18.5 389 2.0 1.1 0.51 14

admission
At 142 4.9 15.4 204 2.1 1.2 0.48 32
discharge

Table 2: Serial Urinalysis

Date Protein Blood leucocytes Specific pH Nitrites

gravity
At 1+ trace trace 1.030 6.0 trace
admission
Mid- 2+ 2+ trace 1.015 5.0 Negative
admission
At 1+ 2+ negative 1.015 5.0 Negative
discharge

• No crystals nor stone on urine macroscopy, precluding analysis for stone type.
• 24-hour urinary excretion of calcium: 13.44mg/dL (normal value: 6.8 – 21.3mg/dL)
• FBC: Hb-10.6g/dL, PCV- 27%, MCV- 65fL, MCH- 22pg, WBC- 14,000/µL, Neutrophils-69%,
Lymphocytes-24%, Others-7%, Platelets- 485 x 109. Peripheral blood film (PBF) revealed toxic
granulation in the neutrophils.

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• Urine microscopy, culture and sensitivity (figure 1.1 and 1.2): Appearance- Turbid, WBC-
Numerous, RBC- 16 – 18/hpf, granular casts- 2+, Culture- yielded no growth.

Figure 1.1 Urine microscopy Figure 1.2 Urine microscopy showing

showing numerous pus cells, red granular cast
blood cells, epithelial cells

Blood Culture: yielded no growth

Hepatitis B Surface Antigen screening: Negative
Anti-Hepatitis C virus screening: Negative
Lentiviral screening: Negative

Figure 2.1 Figure 2.2

Abdomino-pelvic ultrasound (Figures 2.1 and 2.2): Normal hepatobiliary system. The spleen, pancreas
and para-aortic areas are within normal limits. Both kidneys are normal in size measuring 11.6cm and
10.6cm on the left and right respectively. They both show brightly echogenic curvilinear structures casting

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distant acoustic shadows, measuring 21mm and 10mm in diameter on the right and left respectively with
associated moderate hydronephrosis bilaterally. These are suggestive of bilateral renal calculi.

Figure 3: Abdominal computerized tomography showing bilateral renal stones and hydronephrosis (axial
view).

Abdominal CT scan (figure 3) : Normal hepato-biliary system, spleen, pancreas and para-aortic areas
are normal. The kidneys are normal in position and size, the right measures 10.74cm and the left 9.60cm
in bipolar length. There is associated bilateral moderate hydronephrosis and hyperdense calculi in the renal
pelvis measuring 1.65cm and 2.09 cm on the left and right respectively. Excretion is delayed bilaterally.
Conclusion: bilateral moderate hydronephrosis secondary to pelvi-ureteric junction obstruction (PUJO)
from calculi.

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Treatment and outcome
She had intravenous levofloxacin, intravenous
fluids, anti-emetics, and analgesics. She was
managed with urologists was requested to do a
radio-isotope renal scan to ascertain differential
renal function, and to have surgical removal of the
stones, but could not afford the test and surgery.
The symptoms however subsided, the urine output
remained adequate at 1.3L to 2.1L daily, and the
serum chemistry improved. She was subsequently
discharged 10 days after presentation and was
followed up at the nephrology and urology clinics.
She presented two months after discharge with
profound lethargy. Physical examination revealed
that she was very pale, afebrile but no pedal
oedema. Her pulse rate was 112beats per minute,
blood pressure was 110/60mmhg, and haemic
murmur on precordial auscultation. Examination of
other systems were essentially normal. The packed
cell volume was 17%. serum urea of 16.7mmol/L,
creatinine of 287µmol/L with estimated glomerular
filtration rate of 20ml/min/1.73m2. She was
managed as severe anaemia in patient with CKD
secondary to obstructive nephropathy from
nephrolithiasis.
She had 3 units of blood, and the PCV improved to
28%. She was then commenced on parenteral iron
and subcutaneous erythropoietin.
Discussion
The global prevalence of nephrolithiasis and
chronic kidney disease (CKD) have been on the rise
in the last few decades.1 Both conditions are
estimated to affect 5 – 12% and 11.7 – 15.1% of the
world’s population respectively.2,3,4 In the Nigerian
population, nephrolithiasis which was once thought
to be rare is also on an upward trend presumably
due to dietary modifications, climatic changes and
increased urbanization and diagnostic health
facilities.5 Likewise, the prevalence of chronic
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Olanrewaju et al
kidney disease has also increased.6 In the past, the
link between kidney stones and CKD was thought
to be due to the high prevalence of obesity, diabetes
or hypertension in stone formers which are also
established risk factors for chronic kidney disease.1
However, recent data suggests that nephrolithiasis
is an independent risk factor for chronic kidney
disease and end-stage renal disease.1,9 The
highlighted case was a woman who was neither
obese (body mass index was 18kg/m2) nor was she
hypertensive or diabetic, but had recurrent urinary
tract infections.
The association between nephrolithiasis and
acute kidney injury is well established, usually due
to obstructive uropathy or urinary tract infection.7
However, several studies have reported that patients
with nephrolithiasis have a 2-fold increased risk of
declining renal function and need for renal
replacement therapy.8 The third National Health
and Nutrition Examination Survey (NHANES III)
found that patients with nephrolithiasis had a
3.4ml/min lower GFR compared with their
counterparts without kidney stones.10 Also, a
population-based study of the Rochester
Epidemiologic Project reported that patients with
kidney stones had 25–44% increased risk of CKD.11
In addition, the Alberta Kidney Disease Network
database showed that any episode of nephrolithiasis
during an 11-year follow-up was associated with
increased risk of subsequent ESRD (hazard ratio
2.16), CKD (hazard ratio 1.74), or doubling of
serum creatinine (hazard ratio 1.94).12 The
identified potential risk factors for nephrolithiasis-
associated chronic kidney disease include metabolic
diseases such as obesity and diabetes anatomical
anomalies such as hydronephrosis, recurrent
urinary tract infections, female gender, and
hereditary disorders. 1,13
The pathogenetic mechanisms underlying
nephrolithiasis induced CKD have been elucidated
in both animal and human models.1,8 In rat models,
unilateral ureteral obstruction leads to increased
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intratubular pressure which is followed by intense
renal vasoconstriction via the tubule-glomerular
feedback mechanism.14 This results in a decline in
renal blood flow and concomitant drop in the GFR.
If the ureteral obstruction persists with the
associated renal hypoperfusion, glomerulosclerosis,
interstitial fibrosis and nephron dropout ensue,
eventually leading to CKD.14 In addition, urinary
obstruction leads to up-regulation of the
inflammatory cytokines; transforming growth
factor-beta (TGF-β), tumour necrosis factor-alpha
(TNF-α) which stimulate interstitial matrix
expansion, cellular infiltration by fibroblasts and
macrophages which perpetuate tubule-interstitial
inflammation and fibrosis.1,8 Recurrent
pyelonephritis as it occurred in our patient can also
lead to repeated interstitial inflammation, papillary
necrosis and renal scarring.15 Another pathogenetic
mechanism appears to be related to the specific
stone type. Calcium oxalate crystals have been
demonstrated to directly injure the renal tubular
epithelial cells.16,17 They induce mitochondrial
dysfunction with release of reactive oxygen species
and intense inflammatory reaction which results in
apoptosis, tubular necrosis, elaboration of pro-
inflammatory cytokines, and neutrophilic
17,18
infiltration of the interstitium. Additionally,
calcium phosphate stones (brushite stones) have
been associated with the deposition of interstitial
apatite plaques (Randall’s plaques), intra-ductal
plugging and resultant tubular atrophy and cortical
fibrosis.19
This index case had recurrent renal colic and
pyelonephritis for about a decade. Early
presentation and treatment might have prevented
development of CKD. CKD exerts a high burden of
morbidity, mortality, and economic hardship on
individuals, families, and the nations, such that
early identification of its risk factors, like
nephrolithiasis is imperative for prompt
intervention, which may prevent onset of CKD, and
progression to end-stage kidney disease (ESKD).
Nigerian Stethoscope. Vol. 4(2)
Olanrewaju et al
In conclusion, recent evidence has shown a
consistent relationship between nephrolithiasis and
an increased risk of CKD and ESRD. The risk of
CKD from nephrolithiasis is independent of other
established risk factors such as obesity, diabetes and
hypertension. Given the prevalence of kidney
stones in Nigeria, early presentation and treatment
may prevent inception of CKD and its progression.
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