scholarly journals Determining Risk Factors for Triple Whammy Acute Kidney Injury

2021 ◽  
Author(s):  
Jessica Leete ◽  
Carolyn Wang ◽  
Francisco Lopez-Hernandez ◽  
Anita Layton
Keyword(s):  
Acute Kidney Injury ◽  
Computational Models ◽  
Enzyme Inhibitor ◽  
Nervous Activity ◽  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Sympathetic Nervous Activity ◽  
Physiological Factors ◽  
Concurrent Use ◽  
Individual Variations

Concurrent use of a diuretic, a renin-angiotensin system (RAS) inhibitor, and a non-steroidal anti-inflammatory drug (NSAID) significantly increases the risk of acute kidney injury (AKI). This phenomenon is known as "triple whammy". Diuretics and RAS inhibitors, such as an angiotensin converting enzyme inhibitor or angiotensin receptor blocker, are often prescribed in tandem for the treatment of hypertension, whereas some NSAIDs, such as ibuprofen, are available over the counter. As such, concurrent treatment with all three drugs is common. The goals of this study are to better understand the mechanisms underlying the development of triple whammy AKI and to identify physiological factors that may increase an individual's susceptibility. To accomplish these goals, we utilize computational models of long-term blood pressure regulation. These models include variables describing the heart and circulation, kidney function, sodium and water reabsorption in the nephron and the RAS and are parameterized separately for men and women. Hypertension is modeled as overactive renal sympathetic nervous activity. Model simulations suggest that individual variations in water intake, the myogenic response, and drug sensitivity may predispose patients with hypertension to develop triple whammy-induced AKI.

scholarly journals Acute Kidney Injury Relevant to Tubulointerstitial Nephritis with Late-Onset Uveitis Superimposed by Thrombotic Microangiopathy: A Case Report and Review of the Literature

2020 ◽  
Vol 6 (6) ◽  
pp. 414-421
Author(s):  
Youlu Zhao ◽  
Junwen Huang ◽  
Tao Su ◽  
Zhikai Yang ◽  
Xizi Zheng ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Thrombotic Microangiopathy ◽  
Tubulointerstitial Nephritis ◽  
Late Onset ◽  
Drug Hypersensitivity ◽  
Oral Prednisone ◽  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Renal Recovery

<b><i>Background:</i></b> The syndrome of tubulointerstitial nephritis and uveitis (TINU) is an uncommon and multisystemic autoimmune disorder. This review reports a rare case of TINU being superimposed on thrombotic microangiopathy (TMA) and, by comparing with the available literature, also summarizes the clinical features, associated conditions, treatment, and outcome of patients with TINU. <b><i>Summary:</i></b> Herein, we report the case of a 37-year-old male patient with acute kidney injury (AKI) clinicopathologically identified as malignant hypertension-induced TMA superimposed by acute tubulointerstitial nephritis, which was suspected to be related to drug hypersensitivity. After treatment with oral prednisone combined with a renin-angiotensin system inhibitor, the patient achieved partial renal recovery and was withdrawn from hemodialysis. Recurrent AKI concomitant with new-onset asymptomatic uveitis was detected during routine clinical follow-up after cessation of prednisone. TINU was then diagnosed, and prednisone followed by cyclophosphamide was prescribed. The patient achieved better renal recovery than in the first round of treatment and maintained stable renal function afterward. By reviewing the literature, 36 cases were reported as TINU superimposed on other conditions, including thyroiditis, osteoarthropathy, and sarcoid-like noncaseating granulomas. <b><i>Key messages:</i></b> TINU could be complicated by many other conditions, among which TMA is very rare. When presented as AKI, kidney biopsy is important for differential diagnosis. The case also shows that recurrent AKI with concomitant uveitis after prednisone withdrawal strongly suggested the need for long-term follow-up and elongated prednisone therapy for TINU syndrome.

Splanchnic vasoconstriction in heat-stressed men: role of renin-angiotensin system

1982 ◽  
Vol 52 (6) ◽  
pp. 1438-1443 ◽  
Author(s):  
P. Escourrou ◽  
P. R. Freund ◽  
L. B. Rowell ◽  
D. G. Johnson
Keyword(s):  
Heat Stress ◽  
Arterial Pressure ◽  
Nervous Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Sympathetic Nervous Activity ◽  
Plasma Norepinephrine ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Norepinephrine Concentration

We conducted a two-part study to determine whether the renin-angiotensin system contributes to the rise in splanchnic vascular resistance (SVR) during heat stress (rectal temperature was raised 1 degree C). In experiment 1 (control) seven men on a normal salt diet were directly heated (water-perfused suits) for 40–50 min. Arterial pressure (85 Torr) was unchanged; plasma renin activity (PRA) rose from 102 to 239 ng angiotensin I.100 ml-1.3 h-1; and SVR increased 73% (from 63 to 109 units). Experiment 2 was a repetition of experiment 1 on the same subjects, except that propranolol (10 mg iv) was given at the onset of heating to block renin release. Propranolol attenuated the rise in heart rate and reduced mean arterial pressure from 82 to 72 Torr; it blocked the rise in PRA with heating in two subjects, reduced it in three, but increased it in two. Although changes in SVR paralleled those in PRA in three subjects, SVR still rose 60% (from 58 to 99 units) after PRA rise was blocked. In both experiments, plasma norepinephrine concentration rose indicating increased sympathetic nervous activity. During mild heat stress, increased PRA is not a major factor in the increase of SVR.

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