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John Bukowy, Ph.D. - Milwaukee School of Engineering. Milwaukee, WI, US

John Bukowy, Ph.D.

Assistant Professor | Milwaukee School of Engineering


Dr. John Bukowy's area of expertise include software development and machine learning.








Humanizing Machine Learning

Education, Licensure and Certification (3)

Ph.D.: Physiology, Medical College of Wisconsin 2018

M.S.: Electrical Engineering, Illinois Institute of Technology 2012

B.S.: Biomedical Engineering, Marquette University 2008


Dr. John Bukowy is an assistant professor in MSOE's Electrical Engineering and Computer Science Department where he teaches courses in computer science, software development and machine learning. He joined the faculty in 2019. Before joining academia, he worked as a lead quality assurance engineer for MERGE Healthcare.

Accomplishments (3)

Best Graduate Student Award

Cardiovascular Research Center Retreat, Medical College of Wisconsin, 2017

Trainee Travel Award

SRC Renal Hemodynamics Conference, Big Sky, Montana, 2016

American Heart Association Predoctoral Fellowship

Medical College of Wisconsin , 2016

Affiliations (2)

  • American Heart Association : Member
  • Biomedical Engineering Society (BMES) : Member


Event and Speaking Appearances (1)

Ultrasound indicator dilution quantifies renal blood flow distribution in salt-resistant and salt-sensitive rat model of hypertension

FASEB Renal Hemodynamics and Cardiovascular Function in Health and Disease  Big Sky, Montana, 2016

Research Grants (1)

T32 NIH Training Grant

Medical College of Wisconsin $40,320

2015 - 2016

Selected Publications (5)

Progression of diabetic kidney disease in T2DN rats

American Journal of Physiology. Renal Physiology

Palygin, O., Spires, D., Levchenko, V., Bohovyk, R., Fedoriuk, M., Klemens, C.A., Sykes, O., Bukowy, J.D., Cowley Jr, A.W., Lazar, J., Ilatovskaya, D.V.

2019 Diabetic kidney disease (DKD) is one of the leading pathological causes of decreased renal function and progression to end-stage kidney failure. To explore and characterize age-related changes in DKD and associated glomerular damage, we used a rat model of type 2 diabetic nephropathy (T2DN) at 12 weeks and older than 48 weeks. Then we compared their disease progression with control non-diabetic Wistar and diabetic Goto-Kakizaki (GK) rats. During the early stages of DKD, T2DN and GK animals revealed significant increases in blood glucose and kidney-to-body weight ratio. Both diabetic groups had significantly altered renin-angiotensin-aldosterone system function. Then, during the later stages of the disease's progression, T2DN rats demonstrated a remarkable increase in renal damage compared with GK and Wistar rats, as indicated by renal hypertrophy, polyuria accompanied by decrease in urine osmolarity, high cholesterol, a significant prevalence of medullary protein casts, and severe forms of glomerular injury. Urinary nephrin shedding indicates a loss of a glomerular slit diaphragm, which also correlates with the dramatic elevation in albuminuria and loss of podocin staining in aged T2DN rats. Furthermore, we used scanning ion microscopy (SICM) topographical analyses to detect and quantify the pathological remodeling in podocyte foot projections of isolated glomeruli from T2DN animals. In summary, T2DN rats developed renal and physiological abnormalities similar to clinical observations in human patients with DKD, including progressive glomerular damage and a significant decrease in RAAS plasma levels, indicating these rats are an excellent model for studying the progression of renal damage in type 2 DKD.

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Therapeutic Suppression of mTOR (Mammalian Target of Rapamycin) Signaling Prevents and Reverses Salt-Induced Hypertension and Kidney Injury in Dahl Salt-Sensitive Rats


Kumar, V., Evans, L.C., Kurth, T., Yang, C., Wollner, C., Nasci, V., Zheleznova, N.N., Bukowy, J., Dayton, A., Cowley Jr, A.W.

2018 mTOR (mammalian target of rapamycin) signaling has emerged as a key regulator in a wide range of cellular processes ranging from cell proliferation, immune responses, and electrolyte homeostasis. mTOR consists of 2 distinct protein complexes, mTORC1 (mTOR complex 1) and mTORC2 (mTOR complex 2) with distinct downstream signaling events. mTORC1 has been implicated in pathological conditions, such as cancer and type 2 diabetes mellitus in humans, and inhibition of this pathway with rapamycin has been shown to attenuate salt-induced hypertension in Dahl salt-sensitive rats. Several studies have found that the mTORC2 pathway is involved in the regulation of renal tubular sodium and potassium transport, but its role in hypertension has remained largely unexplored. In the present study, we, therefore, determined the effect of mTORC2 inhibition with compound PP242 on salt-induced hypertension and renal injury in salt-sensitive rats. We found that PP242 not only completely prevented but also reversed salt-induced hypertension and kidney injury in salt-sensitive rats. PP242 exhibited potent natriuretic actions, and chronic administration tended to produce a negative Na+ balance even during high-salt feeding. The results indicate that mTORC2 and the related downstream associated pathways play an important role in regulation of sodium balance and arterial pressure regulation in salt-sensitive rats. Therapeutic suppression of the mTORC2 pathway represents a novel pathway for the potential treatment of hypertension.

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Region-Based Convolutional Neural Nets for Localization of Glomeruli in Trichrome-Stained Whole Kidney Sections

Journal of the American Society of Nephrology

Bukowy, J.D., Dayton, A., Cloutier, D., Manis, A.D., Staruschenko, A., Lombard, J.H., Woods, L.C.S., Beard, D.A., Cowley, A.W.

2018 Background: Histologic examination of fixed renal tissue is widely used to assess morphology and the progression of disease. Commonly reported metrics include glomerular number and injury. However, characterization of renal histology is a time-consuming and user-dependent process. To accelerate and improve the process, we have developed a glomerular localization pipeline for trichrome-stained kidney sections using a machine learning image classification algorithm.

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Inhibition of Mammalian Target of Rapamycin Complex 1 Attenuates Salt-Induced Hypertension and Kidney Injury in Dahl Salt-Sensitive Rats


Kumar, V., Wollner, C., Kurth, T., Bukowy, J.D., Cowley Jr, A.W.

2017 The goal of the present study was to explore the protective effects of mTORC1 (mammalian target of rapamycin complex 1) inhibition by rapamycin on salt-induced hypertension and kidney injury in Dahl salt-sensitive (SS) rats. We have previously demonstrated that H2O2 is elevated in the kidneys of SS rats. The present study showed a significant upregulation of renal mTORC1 activity in the SS rats fed a 4.0% NaCl for 3 days. In addition, renal interstitial infusion of H2O2 into salt-resistant Sprague Dawley rats for 3 days was also found to stimulate mTORC1 activity independent of a rise of arterial blood pressure. Together, these data indicate that the salt-induced increases of renal H2O2 in SS rats activated the mTORC1 pathway. Daily administration of rapamycin (IP, 1.5 mg/kg per day) for 21 days reduced salinduced hypertension from 176.0±9.0 to 153.0±12.0 mm Hg in SS rats but had no effect on blood pressure salt sensitivity in Sprague Dawley treated rats. Compared with vehicle, rapamycin reduced albumin excretion rate in SS rats from 190.0±35.0 to 37.0±5.0 mg/d and reduced the renal infiltration of T lymphocytes (CD3(+)) and macrophages (ED1(+)) in the cortex and medulla. Renal hypertrophy and cell proliferation were also reduced in rapamycin-treated SS rats. We conclude that enhancement of intrarenal H2O2 with a 4.0% NaCl diet stimulates the mTORC1 pathway that is necessary for the full development of the salt-induced hypertension and kidney injury in the SS rat.

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Increased Perfusion Pressure Drives Renal T-Cell Infiltration in the Dahl Salt-Sensitive Rat


Evans, L.C., Petrova, G., Kurth, T., Yang, C., Bukowy, J.D., Mattson, D.L., Cowley Jr, A.W.

2017 Renal T-cell infiltration is a key component of salt-sensitive hypertension in Dahl salt-sensitive (SS) rats. Here, we use an electronic servo-control technique to determine the contribution of renal perfusion pressure to T-cell infiltration in the SS rat kidney. An aortic balloon occluder placed around the aorta between the renal arteries was used to maintain perfusion pressure to the left kidney at control levels, ≈128 mm Hg, during 7 days of salt-induced hypertension, whereas the right kidney was exposed to increased renal perfusion pressure that averaged 157±4 mm Hg by day 7 of high-salt diet. The number of infiltrating T cells was compared between the 2 kidneys. Renal T-cell infiltration was significantly blunted in the left servo-controlled kidney compared with the right uncontrolled kidney. The number of CD3(+), CD3(+)CD4(+), and CD3(+)CD8(+) T cells were all significantly lower in the left servo-controlled kidney. This effect was not specific to T cells because CD45R(+) (B cells) and CD11b/c(+) (monocytes and macrophages) cell infiltrations were all exacerbated in the hypertensive kidneys. Increased renal perfusion pressure was also associated with augmented renal injury, with increased protein casts and glomerular damage in the hypertensive kidney. Levels of norepinephrine were comparable between the 2 kidneys, suggestive of equivalent sympathetic innervation. Renal infiltration of T cells was not reversed by the return of renal perfusion pressure to control levels after 7 days of salt-sensitive hypertension. We conclude that increased pressure contributes to the initiation of renal T-cell infiltration during the progression of salt-sensitive hypertension in SS rats.

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