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Abstract

Chronic kidney disease is one of the leading causes of death of captive cheetahs and can cause dramatic changes in lifespan and reproductive success (Mitchell et al., 2018; Terio et al., 2018). In normal function, the kidney provides homeostasis to the body through the filtering of blood. This process removes nitrogenous waste from the body, regulates levels of electrolytes, and controls water balance in the body. When the kidney is not functioning properly, harmful waste and fluids build up in the body and can lead to severe complications such as anemia, high blood pressure, and heart disease (Cleveland Clinic; Temple Health). Clinical signs of chronic kidney disease include but are not limited to dehydration, vomiting, inappetence, weakness, increase in urine output (polyuria), and elevated levels of nitrogenous waste products (azotemia) (Mitchell et al., 2018; Terio et al., 2018). 

The Cheetah Conservation Fund (CCF) is a leading conservation organization in Otjiwarongo, Namibia, that was started in 1990. CCF has resident cheetahs that were orphaned at a young age and are unable to live in the wild because they didn’t learn natural instincts and hunting from their mothers, as well as temporary resident wild cheetahs that are screened for health before being collared for tracking and released back into the wild. Many aspects of CCF contribute to the education and protection of cheetahs throughout Africa. There are locations in Namibia and Somaliland, as well as countless support branches in other countries throughout the world. CCF is a leading research organization for cheetahs and other Namibian animals like caracals, brown hyenas, and African wild dogs, focusing its work on diet, genomic information, and much more. 

With funding from the International Research Opportunities Program (IROP) at the �鶹app, in summer 2025 I conducted a study on kidney disease at the CCF. An on-site veterinarian conducted postmortem examinations on previously deceased cheetahs so that we could evaluate kidney histopathology for concrete structural evidence of disease. We compared these results with bloodwork values to establish a correlation between the stages of kidney failure and the presence of certain biomarkers. The goal was to examine the relationship between urea, creatinine, and SDMA, which are all important biomarkers that help diagnose kidney disease.  Increased knowledge of this relationship could allow for earlier detection and supportive care for cheetahs with kidney disease, thereby extending their lifespan and quality of life. 

Background 

In a twenty-year retrospective analysis, a high number of kidney lesions were observed in captive cheetahs during early necropsy examinations (Munson et al., 1999), which was later confirmed to be a major cause of mortality in these individuals (Bolton & Munson, 1999; Terio et al., 2018). Some studies have suggested that factors including age, stress in captivity, high-protein diets, and even genetics may play a role in predisposing individuals to developing kidney failure (O’Brien et al., 1985). When a cheetah is diagnosed with kidney disease, the management is typically fluid therapy, kidney specific diets, and a reduced protein/calcium intake. Because kidney disease is not curable, the only option is supportive management (Mitchell et al., 2018). 

The author with a cheetah at CCF.

At the CCF, the clinic team prioritizes early detection and supportive care. Routine health checks based on diagnosis history include serum chemistry panels and urinalysis (Lamglait & Vandenbunder-Beltrame, 2017; Terio et al., 2004; Waugh et al., 2018). While all resident cheetahs are brought into the veterinary clinic for a yearly workup, individuals with medical diagnoses are brought in more frequently to monitor vitals and blood values. The supportive treatment includes specialized kidney support diets, fluid therapy, and routine bloodwork to monitor for the blood biomarkers that indicate the severity of their kidney failure (Mitchell et al., 2018; Terio et al., 2004). Because of genetic similarity in captive cheetahs, there may be future research in alternative treatments such as kidney transplants, but currently these options are theoretical (O’Brien et al., 1985). 

The standard measure of kidney function is determined by the glomerular filtration rate, which is how fast the kidney filters waste from the blood (Lamglait & Vandenbunder-Beltrame, 2017). The nephron, which is the fundamental structure of the kidney, comprises the glomerulus and a complex filtration system. When blood enters the glomerulus, a cluster of capillaries around the end of a kidney tubule, the nephron filters plasma, and secretion and reabsorption occur to ensure the fluid and solute levels remain balanced. A chemical by-product called symmetric dimethylarginine (SDMA) is produced during this process and is excreted by the kidneys. 

Historically, creatinine and blood urea nitrogen are the biomarkers considered the “gold standard” for measuring kidney function. However, in some studies it’s been proved that these metrics rise only after approximately 75% of nephron function has been lost because of breakdown of the tissue, whereas SDMA levels can alert to kidney damage at around 40% of nephron loss. Additionally, urea and creatinine can be influenced by external factors such as muscle mass, diet, hydration, and some treatment methods (Lamglait & Vandenbunder-Beltrame, 2017; Waugh et al., 2018). These external factors cause the urea and creatinine to be less indicative of the kidney function. The SDMA value hasn’t been found to be affected by these external factors, which has led to SDMA being used in other species as a more reliable biomarker for measuring kidney function. 

The two most common types of kidney disease are glomerulosclerosis and amyloidosis. While both affect the functioning of the kidney, they have different causes, presentation, and treatment. Glomerulosclerosis is the progressive scarring of the glomeruli, along with the thickening of the basement membranes, which leads to overall decreased filtration of the kidneys. Glomerulosclerosis is observed in roughly 67–84% of captive cheetahs but found in only 13% of wild cheetahs. Glomerulosclerosis prevalence increases with age. Amyloidosis is caused when amyloid protein builds up in the medulla and cortex in the kidney and affects the kidney’s normal function. This type of kidney disease is often linked to chronic inflammation including chronic gastritis, which can contribute to the buildup of amyloid (Bolton & Munson, 1999; Papendick et al., 1997; Terio et al., 2018). Unlike glomerulosclerosis, amyloidosis is less age-linked. 

Oxalate nephrosis, which is another kidney lesion, has been reported to be associated with amyloidosis and interstitial nephritis, but shows an inverse relationship with glomerulosclerosis (Mitchell et al., 2017). In clinical effects, glomerulosclerosis will present with protein in the urine and a gradual glomerular filtration rate decline, where amyloidosis is indicated by increased urination/drinking and a rapid glomerular filtration rate decline. While treatment for both are supportive, the treatment for glomerulosclerosis focuses on managing hypertension and diet, and amyloidosis treatment focuses more on managing inflammation (Bolton & Munson, 1999; Papendick et al., 1997; Terio et al., 2018). 

Although SDMA, creatinine, and urea reference ranges have been established in cheetahs, there are variations based on population and methodology of testing (Hudson-Lamb et al., 2016; Waugh et al., 2018). Multiple studies have been conducted to prove that SDMA is a reliable indication for glomerular filtration rate and could be used as the best way to evaluate kidney disease (Hudson-Lamb et al., 2016; Lamglait & Vandenbunder-Beltrame, 2017; Waugh et al., 2018; McKenna et al., 2020; Sanchez et al., 2020). Previous studies have deemed SDMA an accurate biomarker to detect kidney failure in other species and this study begins to examine if that is possible in cheetahs as well.

Materials and Methods 

Table 1. Cheetah groupings by severity of kidney breakdown based on kidney histopathology report findings.

The approach to this study was multi-pronged. We started by analyzing the changes in urea, creatinine, and SDMA over the time that samples were collected from Nina, a special case study cheetah who resided at CCF from May 2000 to August 2017. Nina was diagnosed with first-degree kidney failure at the time of her necropsy. We analyzed the blood values over her lifetime at CCF to see if I could establish a trend of how the SDMA progressed along with the other blood levels.  

We also evaluated banked blood samples from sixteen deceased cheetahs that were in different stages of kidney disease when they died. All samples were collected by previous CCF staff from the caudal vein on the side of each cheetah’s tail. These samples were stored in a walk-in freezer for varying amounts of time before being thawed for our analysis of urea, creatinine, and SDMA values. We used the IDEXX Catalyst One Veterinary Blood Chemistry Analyzer in conjunction with chemistry slides to measure the amount of each biomarker present in the sample at the time of collection. This analyzer uses a dry-slide technique, where enzymatic and colorimetric reactions on each slide generate an optical signal that indicates the concentration of each biomarker being analyzed. The analyzer machine measures these reactions and converts the results to a quantitative value for us to use. SDMA values, along with urea and creatinine, have been found to stay consistent even through the freeze-thaw cycles required for use of stored samples in chemistry analysis (Lamglait & Vandenbunder-Beltrame, 2017). 

In addition to the blood diagnostics, kidney samples of all cheetahs were sent to Dr. Emily Mitchell and Dr. Karen Terio, two expert cheetah pathologists, who processed, stained, and interpreted the histopathology samples to provide context between the extent of tissue damage and the three kidney biomarkers. 

Results of Kidney Histopathology

Figure 1. Scan of Blondie’s (AJU 1203) kidney with a Masson’s Trichrome stain. The renal cortex is shown with multiple bands of fibrosis throughout the slide.

With the help of Dr. Karen Terio, the sixteen cheetahs from the cross-sectional part of the study were organized into four groups based on the severity of kidney breakdown when examined under the stain and microscope. The resulting groups had five cheetahs in the “mild” group, two cheetahs in the “minimal” group, three cheetahs in the “moderate” group, and six cheetahs in the “severe” group. (Table 1) 

The kidney samples were processed and stained in three different protocols to get a whole picture. Masson’s Trichrome is used to highlight collagen in blue to identify scarring and chronic damage in kidney tissue. (Figure 1) Hematoxylin and Eosin (HE) stain is used to give an overall view of the kidney, with nuclei showing in blue and cytoplasm showing in pink. This allows us to look at the structure and pathology of the tissue in a more general way. The Periodic acid-Schiff (PAS) stain is used to highlight the carbohydrates and basement membrane structures in a bright magenta to be seen more clearly. Using PAS, we can identify if these basement structures have been thickened from chronic disease or inflammation. (Figure 2) 

Figure 2. Scan of Polly’s (AJU 1582) kidney with a PAS stain. Mild segmental thickening of glomerular basement membranes distant from areas of fibrosis.

Nina’s kidney tissue showed accumulations of fibrosis (scar tissue) and small clusters of immune cells like lymphocytes and plasma cells throughout the kidney. These both indicate ongoing inflammation in her kidneys. There were fewer normal tubules, and the glomeruli (filtering units of the kidney) were shrunken and damaged. This shows that her kidneys were unable to filter blood efficiently. There was evidence of a prior but healed bacterial kidney infection as well as mild damage to the glomerular membranes. These findings show that chronic kidney disease was present from the long-term damage, scarring, and loss of function in Nina’s kidneys. 

Results of Biomarker Analysis

The first blood samples we examined were from Nina. Her first medical exam took place on February 26, 2001, and we used blood samples collected between then and August 2017 to analyze SDMA over her lifetime. Nina was diagnosed with first-degree renal failure on her necropsy exam, with the clinical veterinarian noting that the kidneys were pale, smooth, and firm. Nina had one sibling who never exhibited any rise in urea or creatinine and died from a cause unrelated to kidney function. 

Figure 3. Blood values of SDMA, urea, and creatinine over time for Nina. 

Nina’s blood samples from February 1, 2001, through June 12, 2016, all show urea and creatinine blood values to be within a normal range (Hudson-Lamb et al., 2016). In contrast, Nina’s blood sample from July 3, 2017, just a month before her death, shows an elevated level of urea and creatinine that is outside the normal range. When looking at SDMA values in Nina’s blood over time, we saw a slight spike in the blood sample taken on August 30, 2007. This value then wavered before dropping in the blood sample taken on June 12, 2016. 

A trendline was calculated for each biomarker, with a slope to indicate correlation between time and each biomarker as well as an R² value to indicate how well the trendline represents the data. Figure 6 shows that the relationships for urea and creatinine over time are positive and the relationship for SDMA over time is negative. All three R²s indicate a very weak relationship between the biomarkers and time. 

The results from the case study are somewhat unexpected, especially the lack of strong increasing trend in the SDMA biomarker over time. Despite Nina being diagnosed with mild kidney disease at the time of her necropsy, the urea and creatinine levels remained within the normal ranges during the majority of her life. The sharp increase in urea and creatinine before her death likely indicate rapid decline in her kidney function. The SDMA fluctuated over time and shows a weak relationship. This could reflect biological variability, environmental influences, or even a species-specific difference in the reliability of SDMA to indicate kidney disease. The irregular timing of sample collections may also cause errors in the results.  

For each of the sixteen cheetahs in the cross-sectional part of the study, we analyzed a blood sample taken before death for urea, creatinine, and SDMA levels. Figure 7 displays the data for the three blood biomarkers present in each of these samples. There are horizontal lines indicating the found reference ranges for urea and creatinine. Because SDMA has not been studied enough to establish a reference range, there is not a line indicating one. Each cheetah individual is represented separately in the figure and grouped based on their severity of breakdown shown in their histopathology slides. This data shows that overall, as the severity of kidney disease increased, urea and creatinine levels increased as well. (Figure 7) 

Figure 4. Blood values of SDMA, urea, and creatinine for sixteen cheetahs. In this table we combined the minimal and moderate groups because they were so small and because the criteria from the histopathology reports was very similar.  

We calculated the mean and standard deviation for each biomarker in each group cluster. An ANOVA test was then run to determine the statistical significance of each biomarker between the severity groups. For all three biomarkers, the ANOVA test did not reveal a statistical difference among groups. These results were unexpected, because previous studies in cheetahs and other species have shown these three biomarkers increase as kidney function decreases. These results could be caused by a small sample size, high variability between groups, and timing of bloodwork in relation to death.

Discussion 

This research is important to conservation of cheetahs because it provides more insight into how the SDMA biomarker relates to differing levels of kidney failure in captive cheetahs. Future studies would allow for a better establishment in SDMA reference ranges and allow conservation organizations to diagnose kidney disease earlier in cheetahs, allowing for better preventive care and extension of lifespans in captive cheetahs. 

There are a few key limitations and areas for error in this study that could theoretically skew the results. The first would be that the samples were collected over multiple years. Although I ran most of the SDMA levels myself, the other values could have slight variations because they were run on different machines at different labs. Another limitation is that most of the samples were run through the IDEXX Catalyst One machine and a few were run as assays. These two methods use different analytical methods, which could add variation and complicate comparability between samples. 

Future research can be done to better understand what causes or increases risk and severity of kidney failure in cheetahs. A genetic mutation has been identified in some domestic cats with oxalate nephrosis, and this could be researched in cheetahs to establish if this mutation is common in all feline species (Mitchell et al., 2017). Another research topic could explore how diet affects the functioning of kidneys. Lifestyle changes when in captivity could also affect kidney function. Some of these changes include more consistent, high values of calcium and protein in these cheetahs’ diets, which can affect how the kidneys function over time (Lamglait & Vandenbunder-Beltrame, 2017). More diet research on how these elements affect kidney function is vital to understanding how captive environments affect normal organ function. 

In other species, kidney transplants have been successful in treating severe kidney disease. Because of a lack of genetic diversity in the cheetah species, these transplants would likely be highly successful and a possible option for future research to prolong lifespans in our captive cheetahs (Fleck et al., 2003). A limitation to this would be the recovery, because the animals would need to be kept to confined movement and daily antiseptic treatment to avoid infection at the surgery site. 

Cultural Narrative and Conclusion

During my time in Namibia, I lived in dorm-style housing with other interns from many different countries. It was such a unique experience to see how each intern from a different location and with different interests could find their place at CCF. I worked with interns from Namibia, Canada, and all over the US with diverse interests like ecology, zookeeping, livestock management, veterinary technology, media, and more. We were all able to learn from one another through presentations we gave on the different projects we worked on while we were there.

Although my specific research project focused on important biomarkers of kidney disease, I participated in all aspects of conservation during my time at CCF. Every night we received our schedules for the next day, indicating which rotation, or team, we would be working the following day. The rotations included clinic, cheetah keepers, livestock guardian dogs, kraal, horse care, scat dogs, ecology, and creamery team. Cheetah team started at 7:30 a.m. to set up for the cheetah run where a few cheetahs were exercised via a cloth lure attached to a motorized line and rewarded with food. Because my research was in the clinic, I was designated as a clinic intern for five days out of the week. The sixth day of the week was a general day for every intern, where we rotated through the teams to experience other aspects of conservation. I requested a weekly day to work specifically with cheetahs so I could better understand the husbandry of all the cheetahs and the treatments provided to different resident cheetahs in different stages of kidney disease. Each intern got one day off per week, which could be used or saved to take a longer time off for trips to other parts of the country. I took two trips with fellow interns to the coast of Namibia and to Etosha National Park. 

Because of the rotating schedules and different special events popping up, most days at CCF were different. On days I was assigned to the clinic team, I would conduct goat checks at 8:00 a.m. and 4:00 p.m. to ensure our model farm animals did not have any injuries before going out to the field or coming back for the night. The model farm, consisting of goats and sheep, was used to train the livestock guardian dogs and educate farmers in the community. I performed minor treatments such as hoof maintenance, abscess flushing, and wound care out in the field under supervision of the veterinarians or veterinary technician on staff. During the day, we had a mix of activities. Sometimes we performed routine sedated cheetah exams or sperm sample collections, medical procedures for animals on our own or neighboring farms, or other projects given to us from the vets. Every day allowed us to learn something new about how intricate and multifaceted conservation can be. 

Beyond concrete medical or animal protocols and procedures, I learned a lot about the world of conservation and research. I learned how to advocate for myself, how to solve issues to get the best results, and to not get discouraged when things didn’t go to plan. This experience has fueled my passion and commitment to wildlife conservation. I have just been accepted to veterinary school and hope to work in wildlife conservation after graduating. My work with cheetahs has ignited a specific passion for carnivore species. 

This project would not have been possible without the support of many people. I am deeply grateful to my mentor, Dr. Andrew Conroy, for his continued support and guidance. I am also so grateful for the staff at the Cheetah Conservation Fund in Namibia for their assistance with sample processing and data analysis. Finally, I am grateful to the Hamel Center for Undergraduate Research for supporting this project, and to Mr. Frank Noonan, Mrs. Patricia Noonan, Mr. Samuel Paul, and Mrs. Sarah Paul for their generous contributions that made this research possible.

References 

Bolton, L. A., & Munson, L. (1999). Glomerulosclerosis in Captive Cheetahs (Acinonyx jubatus). Veterinary Pathology, 36(1), 14–22.

Cleveland Clinic. Chronic kidney disease. (2023, August 31).

Fleck, C., Schweitzer, F., Karge, E., Busch, M., & Stein, G. (2003). Serum concentrations of asymmetric (ADMA) and symmetric (SDMA) dimethylarginine in patients with chronic kidney diseases. Clinica Chimica Acta, 336(1–2), 1–12. ;

Hudson-Lamb, G. C., Schoeman, J. P., Hooijberg, E. H., Heinrich, S. K., & Tordiffe, A. S. W. (2016). Reference intervals for selected serum biochemistry analytes in cheetahs (Acinonyx jubatus). Journal of the South African Veterinary Association, 87(1). ;

Kirberger, R. M., & Tordiffe, A. S. W. (2017). Ultrasonographically determined renal values and comparisons to serum biochemistry renal variables in aged semi-captive cheetahs (Acinonyx jubatus). BMC Veterinary Research, 13(1), 312. ;

Lamglait, B., & Vandenbunder-Beltrame, M. (2017). Evaluation of symmetric dimethylarginine as an early biomarker of chronic kidney disease in captive cheetahs (acinonyx jubatus). Journal of Zoo and Wildlife Medicine, 48(3), 874–877. ;

McKenna, M., Pelligand, L., Elliott, J., Cotter, D., & Jepson, R. (2020). Relationship between serum iohexol clearance, serum SDMA concentration, and serum creatinine concentration in non‐azotemic dogs. Journal of Veterinary Internal Medicine, 34(1), 186–194. ;

Mitchell, E. P., Church, M. E., Nemser, S. M., Yakes, B. J., Evans, E. R., Reimschuessel, R., Lemberger, K., Thompson, P. N., & Terio, K. A. (2017). Pathology and epidemiology of oxalate nephrosis in cheetahs. Veterinary Pathology, 54(6), 977–985. ;

Mitchell, E. P., Prozesky, L., & Lawrence, J. (2018). A new perspective on the pathogenesis of chronic renal disease in captive cheetahs (Acinonyx jubatus). PLOS ONE, 13(3), e0194114. ;

Munson, L., Nesbit, J. W., Meltzer, D. G., Colly, L. P., Bolton, L., & Kriek, N. P. (1999). Diseases of captive cheetahs (Acinonyx jubatus jubatus) in South Africa: A 20-year retrospective survey. Journal of Zoo and Wildlife Medicine: Official Publication of the American Association of Zoo Veterinarians, 30(3), 342–347. 

O’Brien, S. J., Roelke, M. E., Marker, L., Newman, A., Winkler, C. A., Meltzer, D., Colly, L., Evermann, J. F., Bush, M., & Wildt, D. E. (1985). Genetic basis for species vulnerability in the cheetah. Science, 227(4693), 1428–1434. ;

Papendick, R. E., Munson, L., O’Brien, T. D., & Johnson, K. H. (1997). Systemic AA amyloidosis in captive cheetahs (Acinonyx jubatus). Veterinary Pathology, 34(6), 549–556. ;

Sanchez, C. R., Hayek, L.-A. C., Carlin, E. P., Brown, S. A., Citino, S., Marker, L., Jones, K. L., & Murray, S. (2020). Glomerular filtration rate determined by measuring serum clearance of a single dose of inulin and serum symmetric dimethylarginine concentration in clinically normal cheetahs (Acinonyx jubatus). American Journal of Veterinary Research, 81(4), 375–380. ;

Temple Health. Chronic kidney disease and failure. (n.d.).

Terio, K. A., Marker, L., & Munson, L. (2004). Evidence for chronic stress in captive but not free-ranging cheetahs (acinonyx jubatus) based on adrenal morphology and function. Journal of Wildlife Diseases, 40(2), 259–266. ;

Terio, K. A., Mitchell, E., Walzer, C., Schmidt-Küntzel, A., Marker, L., & Citino, S. (2018). Diseases impacting captive and free-ranging cheetahs. In Cheetahs: Biology and conservation (pp. 349–364). Elsevier. ;

Waugh, L., Lyon, S., Cole, G. A., D’Agostino, J., Cross, J., Strong-Townsend, M., Yerramilli, M., Li, J., Rakitin, A., Hardy, S., & Brandão, J. (2018). Retrospective analysis and validation of serum symmetric dimethylarginine (SDMA) concentrations in cheetahs (acinonyx jubatus). Journal of Zoo and Wildlife Medicine, 49(3), 623–631. ;

Author and Mentor Bios

Royce D’Amelio is a senior from Auburn, New Hampshire, majoring in biomedical sciences: pre-veterinary at the �鶹app. Along with being a Resident Assistant through UNH Residential Life and Housing for three years, she cultivated cultures with multiple different student organizations. Serving as the executive director of the Campus Activities Board and in three executive positions in Alpha Phi Omega as well as being a member of other organizations like ASL Club and Pre-Vet Club allowed her to add to her leadership experience in and out of veterinary medicine. She has worked in multiple veterinary settings such as small-animal clinics, the Fairchild Dairy, New Hampshire Veterinary Diagnostic Laboratory, and other internships abroad in zoological medicine and conservation, all of which have continued to ignite her dream of becoming a veterinarian. In August 2026 she will enter the University of Tennessee Knoxville College of Veterinary Medicine.

Andrew Conroy is a professor in the Department of Agriculture, Nutrition, and Food Systems at the �鶹app. A four-time teaching award winner, he has been teaching people how to work with and manage farm animals for thirty-eight years at the college level. Broadly trained in agriculture, he teaches a variety of different animal science courses, with expertise in managing and handling goats, sheep, swine, dairy and beef cattle, and poultry. In 2023 he began teaching a course called Livestock and Wildlife in Namibia. This writing intensive Discovery World Cultures course combines weekly lectures in Durham, with an embedded faculty-led study abroad component in Namibia over spring break. Students explore the economic, geographic, scientific, cultural, and practical aspects of livestock and wildlife management in Namibia. See:  Dr. Conroy’s work in Africa has also led to mentoring many UNH undergraduate students in research abroad, specifically on topics related to conflicts with wildlife and agriculture. Students he has worked with have done research in Namibia, Tanzania, Zambia, South Africa, Uganda, Zimbabwe, Scotland, Ireland, and Australia. See: /���Ա�ܾ�������dzܰ��Բ���/�����Dz�/2025/04/����������-���Dz԰���-�ǰ���󲹲Բ�-��…

Dr. Laurie Marker is the founder and executive director of the (CCF). She began her career working with cheetahs at Wildlife Safari, a wildlife park in the United States. She first traveled to South West Africa (now Namibia) while conducting research into the rewilding of captive-born cheetahs. Dr. Marker’s research proved that cheetahs held in captivity could be taught to hunt but, more importantly, it was during this time she discovered livestock farmers were killing wild cheetah by the hundreds. Without intervention, the future of the species would be in jeopardy. For this reason, Dr. Marker decided to leave her position at the Smithsonian Institution’s New Opportunities and Animal Health Sciences (NOAHS) Center and founded the CCF in 1990. CCF operates two world-class centers: the International Research and Education Centre in Namibia, and the Cheetah Rescue and Conservation Center in Somaliland.

Dr. Anne Schmidt-Küntzel (DVM, PhD) is the assistant director for animal health and research for the Cheetah Conservation Fund (CCF), for which she established the Life Technologies Conservation Genetics Laboratory in 2008. Dr. Schmidt-Küntzel carries out research on a variety of endangered species using techniques ranging from non-invasive genetics to biomedical questions. Her focus is the status of cheetah genetics and its consequences for conservation, and she was a member of the international collaborative research team responsible for mapping the cheetah genome in 2015. Dr. Schmidt-Küntzel shares her time between CCF's International Field Research and Education Centre in Namibia and the Washington D.C., metropolitan area of the United States, where she is a research associate at the Smithsonian Institute.

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