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Hypertensive Kidney Disease” Fit?

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Hypertensive Kidney Disease” Fit? Arch Clin Med Case Rep 2020; 4 (2): 164-179 DOI: 10.26502/acmcr.96550182 Case Report In The Era of Precision Medicine- Where Does the Diagnosis “Hypertensive Kidney Disease” Fit? Sadichhya Lohani MBBS1*, Mohamed G Atta MD, MPH2 1Renal-Electrolyte and Hypertension Division, University of Pennsylvania, Pennsylvania, United States 2Division of Nephrology, The Johns Hopkins University School of Medicine, Maryland, United States *Corresponding Author: Dr. Sadichhya Lohani, Renal-Electrolyte and Hypertension Division, University of Pennsylvania, Pennsylvania, United States, E-mail: [email protected] Received: 20 January 2020; Accepted: 31 January 2020; Published: 02 March 2020 Abstract Hypertension has been labeled as a cause of non-diabetic chronic kidney disease for decades. In today’s era of precision medicine, labeling benign hypertension as the initial etiology for chronic kidney disease might not be accurate. We discuss an example of a 55-year-old African American patient with pathologic findings of nephrosclerosis without history of hypertension. The pathologic findings of nephrosclerosis can be result of obesity, aging, genetic susceptibility and variety of other previously undiagnosed primary renal disease, and hence shouldn’t be automatically mark hypertensive nephrosclerosis. Multiple studies to date have failed to prove or refute causality between benign hypertension and non-diabetic chronic kidney disease. Genome sequencing of non-diabetic kidney diseases have identified mutations in Apolipoprotein L1 gene, MYH9 gene, and uromodulin gene as risk factors for chronic kidney disease. There is no dispute that uncontrolled hypertension leads to progression of kidney disease and that blood pressure should be controlled adequately. The relationship between hypertension and kidney dysfunction should be viewed as an association and broad differential diagnoses should be pursued. Keywords: Hypertensive nephrosclerosis; Benign hypertension; Non-diabetic chronic kidney disease; Genetic diseases of kidney 1. Introduction Hypertensive nephrosclerosis has been described as an important public health problem and a cause for End Stage Kidney disease (ESKD) for decades [1-4]. About 30 million American adults have chronic kidney disease (CKD) Archives of Clinical and Medical Case Reports 164 Arch Clin Med Case Rep 2020; 4 (2): 164-179 DOI: 10.26502/acmcr.96550182 and roughly 32% of American adults with CKD have hypertension [5]. Approximately 6% of patients with essential hypertension have co-existing chronic kidney disease and are at risk for progression to ESKD [6], mechanism of acute kidney injury (AKI) as evidence of end organ damage from malignant hypertension is well understood and recurrent episodes of acute kidney injury with episodes of hypertensive emergency leads to progression of CKD and ESKD. Hypertension also perpetuates the progression of CKD, and hence the importance of controlling the blood pressure to appropriate goal. There is still debate, however, about whether benign essential hypertension causes CKD, or if underlying kidney disease is the cause of hypertension in patients who are labeled as hypertensive nephrosclerosis [7-9]. Apolipoprotein L1 (APOL1) genotype variants and uromodulin gene variants, among other risk factors, are now being increasingly linked to both hypertension and CKD. This should make us re-think and shift our paradigm from hypertension as a cause for CKD to rather a reflection of underlying primary kidney disease. 2. Case Discussion A 55-year-old African American man presented to the hospital with intermittent nausea and fatigue. He was noted to have a creatinine peak of 7.1 mg/dl from his baseline of 2.6-3.2 mg/dL. He had a history chronic kidney disease of unknown etiology for 6 years with serum creatinine of 1.5 mg/dl 4 years prior to presentation. His blood pressure (BP) on presentation was 133/75 mmHg and remained controlled during the seven-day hospital stay with average blood pressure ranging from 113-125/ 60-75 mmHg with occasional systolic readings of 140-150 mmHg. He didn’t have access to regular health care. His body mass index (BMI) was 27 kg/m2. He didn’t have a history of hypertension, diabetes mellitus, coronary artery disease, nephrolithiasis, or pyelonephritis. He had a history of untreated hepatitis C with viral load of 1,115 copies/ml diagnosed a year prior to this presentation. A year prior to this admission, his blood pressure was 125/88 mmHg. There was documentation of one isolated systolic blood pressure of 140 mmHg a year prior. Even prior to the diagnosis of CKD 6 years ago, he didn’t have history of high blood pressure. He was never on any antihypertensive medications in the past. His urine protein: creatinine ratio a year prior to the presentation was 460 mg/g. Home medications included calcium and magnesium supplements for cramps. He had history of chronic back pain. He had remote use of intermittent non-steroidal anti-inflammatory agents (NSAIDS). He was born at term and didn’t have any complications at birth or major illnesses during childhood. He didn’t have a family history of kidney disease or hypertension. He didn’t have history of smoking, alcohol or recreational drugs. He didn’t have history of blood transfusion. He worked as a driver and didn’t have occupational exposure to toxic chemicals or heavy metals. Upon further evaluation, on this admission his 24-hour urine protein was 6.7 g. A kidney ultrasound showed a right kidney measuring 10.7 cm and left kidney measuring 11 cm without hydronephrosis. Urine sediment showed few white cells, non-dysmorphic red cells and many waxy casts per high power field. Complement levels were low, with C3 49 mg/dL (79-152) and C4 13 mg/dL (12-42). Free light chains were normal. Uric acid level was 9.0 mg/dL Archives of Clinical and Medical Case Reports 165 Arch Clin Med Case Rep 2020; 4 (2): 164-179 DOI: 10.26502/acmcr.96550182 (3.5-7.2 mg/dL). Serum protein electrophoresis didn’t reveal monoclonal protein. HIV was negative on ELISA. ANA, rheumatoid factor, cryoglobulins were negative. Lactate dehydrogenase was 324 U/L (118-273) and haptoglobin of 37 mg/dL (36-196mg/dL). In addition to worsening renal function, the proteinuria had worsened from 460mg/g a year prior to 6.7 g on admission. With the initial differential diagnosis of hepatitis C related kidney disease considering proteinuria, hypocomplementemia and history of untreated hepatitis C infection, a kidney biopsy was performed. The biopsy specimen consisted of three cores containing approximately 80% renal cortex and 20% medulla. The biopsy showed 9 glomeruli of which 55% were globally sclerosed. Non-obsolescent glomeruli have prominent periglomerular fibrosis and variable glomerular capillary wall remodeling/reduplication with ischemic type changes. Tubular atrophy and interstitial fibrotic expansion involve approximately 60% of the cortex involves approximately 60% of the cortex. Of the 3 interlobular arteries sampled, severe fibro-intimal thickening, fibroelastosis, medial hypertrophy was noted, arterioles with focal “onion skinning changes with severe luminal constriction suggestive of severe arteriosclerosis and arteriolosclerosis were present. The immunofluorescence (IF) pattern was non-specific not favoring hepatitis C mediated process. Electron microscopy (EM) revealed segmental podocyte foot process fusion (approximately 50%) consistent with secondary focal segmental glomerulosclerosis or FSGS; the glomerular basement membranes were thickened with segmental ischemic type wrinkling. No immune complex type deposits were identified. (Figure 1 and 2). These biopsy findings were reported to be consistent with vascular mediated glomerular injury (glomerular hypoperfusion) secondary to severe chronic renovascular sclerosis. Figure 1: Renal biopsy showing arteriosclerosis on light microscopy (Trichrome and Silver stain). Light microscopy with trichrome (left) and silver stain (right). There is severe fibrointimal thickening, fibroelastosis and medial hypertrophy. Arterioles show focal 'onion-skinning' changes with severe luminal constriction. Significant arteriolar hyalinosis is not appreciated. Archives of Clinical and Medical Case Reports 166 Arch Clin Med Case Rep 2020; 4 (2): 164-179 DOI: 10.26502/acmcr.96550182 Figure 2: Renal biopsy showing global glomerulosclerosis and periglomerular fibrosis on light microscopy (H&E and Trichrome). Light microscopy with H&E(left) and trichrome (right) stain. Globally sclerosed glomeruli seen. Non-obsolescent glomerulus has prominent periglomerular fibrosis. Mesangial matrix is mildly and segmentally expanded with no significant increase in cellularity. There are no crescents, necrosis or thrombi identified. Interestingly, the patient didn’t have history of uncontrolled hypertension which was supported by his blood pressure trends in the hospital and limited blood pressure readings on ambulatory settings. Because ambulatory readings were not possible to obtain due to patient’s lack of routine outpatient care, periodic masked hypertension outside of the hospital would be difficult to obtain. Hence, in addition to close monitoring of his blood pressure in the hospital, work up for secondary causes of hypertension for episodic masked hypertension were pursued. He only had mildly elevated plasma metanephrines at 66 pg/mL (reference <57) with normal normetanephrine level at 142 pg/ml (reference <148). 24-hour urine nor-metanephrine was 351 mcg (reference-122-676 mcg/24hr) and total epinephrine plus norepinephrine
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