ISSN: 2455-5282

Global Journal of Medical and Clinical Case Reports

Case Report       Open Access      Peer-Reviewed

The Dilemma of Fluid Management in Acute Kidney Injury During Sickle Cell Crises: A Case Report

Adebukola Ajite1,2*, Ezra Ogundare1,2, Ademola Fasanmi2 and Benjamin Ilori2

1Ekiti State University, College of Medicine, Department of Paediatrics and Child Health, Ado Ekiti, Nigeria
2Ekiti State University Teaching Hospital, Department of Paediatrics, Ado Ekiti, Nigeria

Author and article information

*Corresponding author: Adebukola Ajite. Kadi, Ekiti State University, College of Medicine, Department of Paediatrics and Child Health, Ado Ekiti, Nigeria, E-mail: [email protected]
doi : 10.17352/gjmccr.000255
Received: 25 May, 2025 | Accepted: 05 June, 2026 | Published: 08 June, 2026
Keywords: Intravascular haemolysis; Sickle cell anaemia; Acute kidney injury; Fluid management

Cite this as

Ajite A, Ogundare E, Fasanmi A, Ilori B. The Dilemma of Fluid Management in Acute Kidney Injury During Sickle Cell Crises: A Case Report. Glob J Medical Clin Case Rep. 2026:13(6):128-131. Available from: 10.17352/gjmccr.000255

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© 2026 Ajite A, et al. 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 author and source are credited.

Abstract

Fluid therapy remains a cornerstone in the management of sickle cell crises, as adequate hydration reduces blood viscosity and limits further sickling. However, in the presence of oliguric Acute Kidney Injury (AKI), fluid administration becomes a delicate balance to prevent volume overload and worsen morbidity. The case is that of an 8-year-old known sickle cell anemic boy who presented with fever and bone pain for 3 days, jaundice, and passage of dark brown urine. He was pale, icteric, and had non-tender hepatomegaly. He was managed for Vaso-occlusive crisis (VOC) and hyperhaemolytic crisis due to presumed sepsis. He had a blood transfusion and was subsequently placed on intravenous fluids 5% Dextrose in 0.9% Saline at 120% of maintenance. He developed Acute Kidney Injury (AKI) with oliguria (urine output 0.3ml/kg/hr), elevated serum urea (17.70mmol/L), creatinine (241.4µmol/L), and hyperkalemia (K 5.58mmol/L) by the following day on admission. His systolic blood pressure ranged from 140 to 100mmHg, while the diastolic ranged from 100mmHg to 60mmHg. In view of the oliguric AKI, the intravenous fluid was reduced to 2/3rd of maintenance fluid using 5% Dextrose Saline, while the remaining 1/3rd was given orally. He was given furosemide with alkalization of the urine. His urine output and vital signs were closely monitored, and hyperkalemia and hypertension were managed appropriately. By the end of the first week of admission, there was significant improvement in renal parameters, and urine output normalized. The blood pressure at discharge was 90/60mmHg. In conclusion, balancing adequate hydration to prevent further sickling must be weighed against the risk of fluid overload and worsening renal dysfunction in co-existing AKI.

Indexing and Abstracting

Introduction

Sickle cell disease (SCD) is an autosomal recessive disorder that is seen more in sub-Saharan Africa [1]. Annually, about 300,000 children are born with sickle cell anaemia globally, and 80% of these children are born in Africa [2,3]. SCD occurs as a result of substitution of glutamate for valine at the sixth amino acid of the beta-globin chain, resulting in haemoglobin S (HbS) tetramers. Sickle cell anaemia (SCA) occurs when there is homozygous inheritance of HbS [1]. This haemoglobin S forms crescent-shaped crystals under instances of low oxygen tension, such as tissue hypoxia, oxidative stress, or dehydration. Accumulation of the HbS can lead to red blood cell sickling, early destruction of erythrocytes (haemolysis), and widespread vaso-occlusive episodes (VOC), subsequently resulting in multiorgan damage [4]. Intravascular haemolysis is a life-threatening condition in SCD, and consequent haemoglobinuria can lead to kidney damage as a result of the toxic effects of free haemoglobin on the kidney tubules, leading to acute kidney injury (AKI) [4].

Acute kidney injury is a potentially reversible sudden deterioration in renal function and is assessed by parameters such as urine output and serum creatinine [5]. The Kidney Disease: Improving Global Outcomes (KDIGO) classification of AKI is based on these two parameters [6]. The aetiologies of AKI in SCA are multifactorial and include haemoglobinuria, sepsis, consequent peripheral vasodilation leading to renal hypoperfusion, and recurrent exposure to non-steroidal anti-inflammatory drugs [7,8]. Haemoglobinuria is a potential intrinsic renal cause of AKI. Severe intravascular haemolysis results in a large burden of haemoglobin, which overwhelms the binding capacity of haptoglobin as well as the degenerative capacity of heme oxygenase [7,8]. The free haemoglobin is nephrotoxic; therefore, adequate hydration is required to maintain renal perfusion and prevent acute kidney injury, while closely monitoring the red blood cell volume for anaemia. However, in AKI with evidence of acute tubular necrosis (ATN) often manifesting as persistent oliguria, failure to respond to fluid administration and diuretics [7], it is paramount to restrict fluid intake in order to prevent circulatory overload.

Here comes the dilemma in fluid management when a sickle cell anaemic patient presents in crisis with obvious need for increased perfusion to (i) ameliorate the incidence of VOC by improving vascular flow, (ii) improve excretion of free haemoglobin, and preserve renal perfusion. If the same patient has a complication of acute kidney injury with the need for fluid restriction to avoid volume overload, the appropriate fluid prescription might pose a challenge. AKI is usually associated with reduced glomerular filtration rate (GFR), which is a risk factor for increased mortality in SCD [9-11]. Kidney disease has been found to account for approximately 16–18% of overall mortality in patients with SCD [12,13]. This case report suggests a need for meticulous review of the fluid prescription in these patients.

Case report

An 8-year-old boy, being managed for sickle cell anemia, presented with fever and bone pain for 3 days. At admission, he was pale, mildly icteric, passing dark urine, and had hepatomegaly. He developed oliguria while on admission with urine output of 0.3ml/kg/hr and facial oedema. He was first diagnosed at 4-years of age. He had a history of recurrent vaso-occlusive crises with an average of 5 – 8 episodes/ year and suboptimal clinical follow-up. Renal evaluation showed elevated urea and creatinine with hyperkalemia, as shown in Table 1, all consistent with AKI.

Investigation results (Tables 1,2)

Table 1: Electrolyte, Urea, and Creatinine (E/U/Cr) progression
E/U/Cr 1ST day of admission 2nd day of admission 4th day of admission 7th day of admission At discharge
Potassium(mmol/L) 5.58 5.08 4.73 5.78 3.64
Sodium (mmol/L) 131.7 125.5 121.7 125.7 140.1
Chloride (mmol/L) 102 98.5 91.6 99.7 99.0
Urea (mmol/L) 17.7 15.9 23.8 19.34 6.98
Creatinine (µmol/L) 241.4 132.4 152.8 107.0 80.8
Table 2: Results of other investigations.
Day Urinalysis Full blood count RBS RDTMP Total serum protein Serum albumin
At admission pH 5 WBC 8.56 x 109/L 93mg/dL negative 65.22g/L 36.53g/L
  Haemoglobinuria Neutrophil 74.1%,        
  Proteinuria + Lymphocyte 16.6%,        
    Haematocrit 21.9%,        
    Platelets 320 x 109 /L        
WBC = White blood cell count, RDTMP = Rapid diagnostic test for malaria, RBS = Random blood sugar Renal ultrasound showed normal-sized kidneys with preserved cortico-medullary differentiation. Blood culture yielded no growth.

Treatment

He was managed for vaso-occlusive crisis (VOC) and hyperhaemolytic crisis presumed to be precipitated by sepsis. He had a blood transfusion. In an attempt to reduce the risk of haemoglobin-induced pigment nephropathy in the index patient, hydration was started at 120% of maintenance using 5% Dextrose saline. Following features of AKI, fluid management proved challenging due to the competing risks of worsening volume overload due to the renal impairment and the need to give adequate fluid to combat VOC. Subsequently, the intravenous fluid was reviewed to daily 100% maintenance fluid, 2/3rd of which was given via intravenous route and the remaining 1/3rd was given as oral. There was a strict input and output chart for close monitoring. Alkalinization of the urine was done by giving the patient intravenous sodium bicarbonate and placing on frusemide 1mg/kg while monitoring the urine output and keeping a urine rack that showed improvement in the urine colour over time. The patient responded to cautious fluid resuscitation and diuretic therapy, with gradual improvement in urine output and renal function. The clinical course was complicated by high blood pressure ranging from systolic 140 to 120mmHg and diastolic 100 to 90mmHg. This was managed with tab aldomet and amlodipine, which were subsequently changed to tab lisinopril on follow-up following resolution of the AKI. The blood pressure at follow up was 90/40mmHg. There was persistence of proteinuria on follow-up, suggesting evolving Sickle Cell Nephropathy.

Discussion

This case highlights the therapeutic challenge of fluid management when there is co-existing AKI and the complex interplay between haemolysis, vaso-occlusion, and renal impairment in a child with sickle cell anaemia. In this patient, the low packed cell volume, jaundice, presence of dark brown urine, oliguria, and biochemical derangements suggest a hyperhaemolytic crisis with intravascular haemolysis and AKI. Free haemoglobin released during haemolysis is nephrotoxic and can precipitate acute tubular necrosis, which may contribute to the development of acute kidney injury [14]. Haemoglobinuria is likely to trigger hydroxyl radical-mediated peroxidation of lipid and acute tubular necrosis [15,16]. The structure of the kidney microvasculature makes the renal medulla susceptible to hypoxia and renal medullary hypoxia from sickling; this may also further promote renal dysfunction [17].

The diagnosis of AKI was made in this patient following the presence of oliguria and rising creatinine, and this necessitated careful monitoring of fluid balance and the introduction of diuretics to promote urine output. Most sickle cell crisis guidelines encourage hydration to reduce sickling [5-7,18], but this patient simultaneously developed oliguric AKI where excessive hydration could worsen fluid overload. This created a therapeutic dilemma.

Fluid therapy remains a cornerstone in the management of sickle cell crises, as adequate hydration reduces blood viscosity, limits further sickling, and reduces pain [18]. The routine administration of extra fluid regardless of the individual’s state of hydration was advocated to be a useful adjunct mode of intervention [18]. However, in the presence of AKI, fluid administration becomes a delicate balance. Excess fluid may lead to volume overload, worsening hypertension, and risk of pulmonary complications such as acute chest syndrome, while inadequate hydration may perpetuate renal hypoperfusion and ongoing sickling [18]. Distinguishing between the need for fluid resuscitation in SCA and restriction of fluid in associated acute tubular necrosis may be difficult [8], however, close attention to features suggestive of acute tubular necrosis, such as persistent oliguria and elevated fractional excretion of sodium (more than 2%), is helpful [8,9]. In this patient, the decision to reduce intravenous fluid to 2/3rd of maintenance was based on the persistent oliguria following initial hydration and risk of impending volume overload. The remaining 1/3rd of the maintenance fluid was administered orally, as the risk of volume overload is low in this route of fluid administration. The gradual improvement in urine output and decline in serum creatinine suggested recovery from acute tubular injury. The successful outcome following reduction of intravenous fluids while maintaining careful monitoring suggests that individualized fluid prescription may be preferable to routine aggressive hydration in selected patients with sickle cell crisis complicated by AKI.

This case emphasizes that fluid management in sickle cell patients with acute kidney injury may sometimes not be protocol-driven but highly individualized. It requires continuous reassessment of clinical status, urine output, and renal parameters. This is in line with the previous documented guideline, which stated that measures to mitigate renal damage should include daily weighing and ensuring fluid balance [20].

Alkalinization of the urine by giving sodium carbonate combined with a loop diuretic was done in the index patient; this might have contributed to the good outcome in this patient, as previously documented that alkalization is effective in pigment-induced AKI secondary to haemoglobinuria [21]. The reason for this could be attributed to the solubility of pigments like haemoglobin in alkaline urine, thereby limiting the risk of cast and crystal formation as well as kidney damage. The urine alkaline medium also impairs the degradation of haemoglobin to heme and free toxin, which have a nephrotoxic effect [17]. The hypertension in this patient might have been related to volume overload, although other contributors, including acute kidney injury itself, cannot be excluded. Lisinopril, an angiotensin converting enzyme inhibitor, was considered following resolution of the acute kidney injury; this is because of its reno-protective impact by reducing proteinuria in sickle cell anaemic patients [22].

To our knowledge, pusblished reports discussing individualized fluid restriction strategies in children with sickle cell crisis complicated by oliguric AKI remain limited, making this case a useful illustration of the challenges clinicians may face. Multidisciplinary care involving hematologists and nephrologists is essential to navigate these challenges.

In conclusion, the co-existence of sickle cell crisis and AKI presents a therapeutic dilemma and underscores the complexity of fluid management where the clinician must balance the need for adequate hydration to prevent vaso-occlusive crisis against the risks of fluid overload, electrolyte disturbances, and worsening of renal dysfunction. The case report is intended to bridge a gap between clinical knowledge and lifesaving action. Early recognition, judicious fluid selection, and close monitoring are critical in improving outcomes and preventing long-term renal sequelae in sickle cell anaemia.

References

  1. Baddam S, Rout P. Sickle Cell Nephropathy. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026-. Updated 2025 Jun 2.
  2. Chakravorty S, Williams TN. Sickle cell disease: a neglected chronic disease of increasing global health importance. Arch Dis Child. 2015;100(1):48-53. Available from: https://doi.org/10.1136/archdischild-2013-303773
  3. McGann PT, Hernandez AG, Ware RE. Sickle cell anemia in sub-Saharan Africa: advancing the clinical paradigm through partnerships and research. Blood. 2017;129(2):155-161. Available from: Sickle cell anemia in sub-Saharan Africa: advancing the clinical paradigm through partnerships and research. Blood. 2017;129(2):155-161 https://doi.org/10.1182/blood-2016-09-702324
  4. Dvanajscak Z, Walker PD, Cossey LN, Messias NC, Boils CL, Kuperman MB, Larsen CP. Hemolysis-associated hemoglobin cast nephropathy results from a range of clinicopathologic disorders. Kidney Int. 2019;96(6):1400-1407. Available from: https://doi.org/10.1016/j.kint.2019.08.026
  5. Kopac M. Acute kidney injury in children: classification, recognition and treatment principles. Children (Basel). 2024;11(11):1308. Available from: https://doi.org/10.3390/children11111308
  6. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2(1):1-138. Available from: https://kdigo.org/wp-content/uploads/2016/10/KDIGO-2012-AKI-Guideline-English.pdf
  7. Holley JL. Clinical approach to the diagnosis of acute renal failure. In: Greenberg A, Cheung AK, Coffman TM, Falk RJ, Jennette JC, editors. Primer on Kidney Diseases. 5th ed. Philadelphia: Saunders Elsevier; 2009. p. 277-283.
  8. Nair RK, Khaira A, Sharma A, Mahajan S, Dinda AK. Spectrum of renal involvement in paroxysmal nocturnal hemoglobinuria: a report of three cases and a brief review of the literature. Int Urol Nephrol. 2008;40(2):471-475. Available from: https://doi.org/10.1007/s11255-008-9356-5
  9. Darbari DS, Onyekwere O, Nouraie M, Minniti CP, Luchtman-Jones L, Rana S, et al. Severe painful vaso-occlusive crises and mortality in a contemporary adult sickle cell anemia cohort study. PLoS One. 2013;8(11):e79923. Available from: https://doi.org/10.1371/journal.pone.0079923
  10. Gladwin MT, Sachdev V, Jison ML, Shizukuda Y, Plehn JF, Minter K, et al. Risk factors for death in 632 patients with sickle cell disease in the United States and United Kingdom. PLoS One. 2014;9(7):e99489. Available from: https://doi.org/10.1371/journal.pone.0099489
  11. Elmariah H, Garrett ME, De Castro LM, Jonassaint JC, Ataga KI, Eckman JR, et al. Factors associated Available from:with survival in a contemporary adult sickle cell disease cohort. Am J Hematol. 2014;89(5):530-535. Available from: https://doi.org/10.1002/ajh.23683
  12. Platt OS, Brambilla DJ, Rosse WF, Milner PF, Castro O, Steinberg MH, et al. Mortality in sickle cell disease. Life expectancy and risk factors for early death. N Engl J Med. 1994;330(23):1639-1644. Available from: https://doi.org/10.1056/nejm199406093302303
  13. Hamideh D, Alvarez O. Sickle cell disease-related mortality in the United States, 1999-2009. Pediatr Blood Cancer. 2013;60(9):1482-1486. Available from: https://doi.org/10.1002/pbc.24557
  14. Deuel JW, Schaer CA, Boretti FS, Opitz L, Garcia-Rubio I, Baek JH, et al. Hemoglobinuria-related acute kidney injury is driven by intrarenal oxidative reactions triggering a heme toxicity response. Cell Death Dis. 2016;7(1):e2064. Available from: https://doi.org/10.1038/cddis.2015.392
  15. Sakthiswary R, Das S, Fadilah SA. Successful treatment of acute kidney injury secondary to haemoglobinuria in paroxysmal nocturnal haemoglobinuria with alkaline diuresis. EXCLI J. 2012;11:198-203.
  16. Tsai CW, Wu VC, Lin WC, Huang JW, Wu MS. Acute renal failure in a patient with paroxysmal nocturnal hemoglobinuria. Kidney Int. 2007;71(11):1187. Available from: https://doi.org/10.1038/sj.ki.5002179
  17. Ullah MM, Basile DP. Role of renal hypoxia in the progression from acute kidney injury to chronic kidney disease. Semin Nephrol. 2019;39(6):567-580. Available from: https://doi.org/10.1016/j.semnephrol.2019.10.006
  18. Okomo U, Meremikwu M. Fluid replacement therapy for acute episodes of pain in people with sickle cell disease. Cochrane Database Syst Rev. 2017;7:CD005406. Available from: https://doi.org/10.1002/14651858.cd005406.pub5
  19. Esson ML, Schrier RW. Diagnosis and treatment of acute tubular necrosis. Ann Intern Med. 2002;137(9):744-752. Available from: https://doi.org/10.7326/0003-4819-137-9-200211050-00010
  20. Atoyebi W. Acute kidney injury in patients with sickle cell disease: clinical guideline. Wessex and Thames Valley Haemoglobinopathy Network, Adult Haemoglobinopathy Service, NHS. Available from: https://nssg.oxford-haematology.org.uk/red-cell/documents/acute-management-sickle-cell-disease/S15-acute-kidney-injury-in-scd.pdf
  21. Ataga KI, Saraf SL, Derebail VK. The nephropathy of the sickle cell trait and sickle cell disease. Nat Rev Nephrol. 2022;18(6):361-377. Available from: https://doi.org/10.1038/s41581-022-00540-9
  22. Aleem A, Al-Sultan A, Sharif M, Alotaibi DS. Response to lisinopril in patients with sickle cell anaemia and proteinuria. Saudi J Kidney Dis Transpl. 2023;34(6):531-536. Available from: https://doi.org/10.4103/sjkdt.sjkdt_312_22
 

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