Introduction: Calcification on native kidney biopsy specimens is often noted by pathologists, but the consequence is unknown. Methods: We searched the pathology reports in the Biopsy Biobank Cohort of Indiana for native biopsy specimens with calcification. Results: Of the 4,364 specimens, 416 (9.8%) had calcification. We compared clinical and histopathology findings in those with calcification (n = 429) compared to those without calcification (n = 3,936). Patients with calcification were older, had more comorbidities, lower estimated glomerular filtration rates (eGFR), were more likely to have hyaline arteriosclerosis, interstitial fibrosis/tubular atrophy, and a primary pathologic diagnosis of acute tubular injury or acute tubular necrosis when compared to patients without calcification. Patients with calcium oxalate deposition alone, compared to calcium phosphate or mixed calcifications, had fewer comorbidities but were more likely to have a history of gastric bypass surgery or malabsorption and take vitamin D. In patients with two or more years of follow-up, multivariate analyses showed the presence of calcification (HR 0.59, 0.38–0.92, p = 0.02) and higher eGFR (HR 0.76, 0.73–0.79, p < 0.001), was associated with decreased likelihood of progressing to end-stage renal disease. The presence of calcification was also associated with a reduced slope/decline in eGFR compared to known biopsy and clinical risk factors for decline in kidney function. We hypothesized this was due to more recoverable acute kidney injury (AKI) and found more severe acute kidney injury network stage in patients with kidney calcification but also greater improvement over time. Discussion/Conclusion: In summary, we demonstrated that calcification on kidney biopsy specimens was associated with a better prognosis than those without calcification due to the association with recoverable AKI.

Calcifications in kidney biopsy specimens are occasionally observed by nephropathologists and are usually localized to the lumina of renal tubules. More rarely, interstitial deposition may be observed in patients with disorders of calcium metabolism such as sarcoidosis or nephrolithiasis. Using polarized light microscopy, tubular calcifications can be differentiated as calcium oxalate (CaOx) (birefringent) or calcium phosphate (non-birefringent). The term “dystrophic” has been used in the literature to denote calcium phosphate deposition calcification due to high calcium-phosphorus product in the blood or urine. However, studies have demonstrated that deposition of brushite or hydroxyapatite (calcium phosphate) in the bone and vasculature is tightly regulated and not simply passive precipitation [1, 2]. In both bone and vascular smooth muscle cells, deposition of calcium phosphate or mineralization, occurs through a tightly regulated set of enzymes that produce mineralized matrix vesicles laden with calcium and phosphorus [3, 4], with the magnitude of calcification balanced by the presence of tissue-specific inhibitors [1]. Thus, non-birefringent calcium phosphate deposition in the kidney may also be in response to disordered mineral metabolism or inhibitors in the kidney tubules rather than passive deposition. In contrast to calcium phosphate deposition, the presence of birefringent CaOx deposition in the kidneys has been observed in patients with excess intestinal absorption of oxalate due to gastric bypass, malabsorption, ethylene glycol toxicity, or impaired metabolism as in primary hyperoxaluria. In addition to kidneys, CaOx deposits can be found in many different tissues [5, 6].

Limited data exist describing the association of renal tubular calcium deposition with clinical risk factors and histopathologic findings. Even less is known about the clinical significance and long-term outcomes of such deposition. The purpose of the present study was to utilize the Biopsy Biobank Cohort of Indiana (BBCI) [7] to systematically assess the incidence of different types of kidney calcium deposits and the clinical risk factors and consequences of such findings.

Study Population

Subjects were retrospectively identified from the BBCI. The BBCI is a biorepository and kidney biopsy report database of 4,364 specimens from subjects who underwent a kidney biopsy with specimen interpretation by the Indiana University Health Pathology between 2001 and 2017 [7]. The biopsy database is linked to the Indiana Patient Care Network, a state-wide patient care network of electronic health records (EHRs), with the Regenstrief Institute serving as honest data broker. Electronic kidney biopsy reports were categorized in a uniform manner as described in detail elsewhere [7]. All native kidney biopsy interpretation reports were then electronically searched for “calci” to find the terms “calcium,” “calcified,” or “calcification.” These were further classified by the type of calcification categorized as one of the following: CaOx (n = 125), dystrophic calcification/calcium phosphate (DC, n = 230), mixed CaOx and dystrophic calcification (DC + CaOx, n = 30), or “other” sites of deposition such as the interstitium with systemic diseases such as sarcoidosis (n = 31). The “other” group was subsequently excluded as the cause of calcification was known.

We first compared demographic, laboratory, and biopsy specimen characteristics at the time of kidney biopsy acquisition from subjects who had (1) no reported calcification (n = 3,936) to any reported calcification (n = 4,364) and (2) CaOx only (n = 125) versus DC only (n = 230). For the longitudinal analyses, only individuals who underwent biopsy between 2001 and 2017 and had a minimum of 2 years of follow-up data including linked clinical, demographic, and outcome were included (n = 3,772). Individuals meeting inclusion criteria were followed longitudinally for up to 5 years or until death, end-stage renal disease (ESRD), or the date of last follow-up based on EHR. The date of first kidney biopsy served as the index date, and the last date of overall follow-up was December 12, 2017. Acute kidney injury (AKI) was defined as an indication for a biopsy or a biopsy report that mentioned acute interstitial nephritis, acute tubular necrosis, cholesterol emboli, pyelonephritis, thrombotic microangiopathy, contrast nephropathy, or sickle cell nephropathy and categorized by acute kidney injury network (AKIN) stage. This study was approved by the Institutional Review Board at the Indiana University School of Medicine, Indianapolis IN (IRB # 1601431846).

Demographic and Clinical Exposure Variables

Demographic variables included age, self-reported race, sex, and smoking history (never, past, or current). Comorbidities included coronary artery disease (CAD), congestive heart failure, diabetes mellitus (DM), and hypertension (HTN) as defined by established computer algorithms developed by the Regenstrief Institute [8-10]. These algorithms utilize elements such as ICD codes, clinical documentation, medication use, and laboratory data to categorize the presence or absence of these conditions in the eligible study population. In the biopsy specimens with calcification, chart review was done by one individual without knowledge of the biopsy specimen interpretation to assess the presence of malabsorption or gastric bypass surgery and use of supplements (vitamin C due to its metabolism to oxalate and vitamin D that enhances calcium absorption).

Laboratory Variables

The estimated glomerular filtration rates (eGFR) at index date and throughout follow-up were calculated according to the CKD-EPI creatinine formula [11]. Proteinuria was obtained from the 24 h urine protein collection or spot urine protein/creatinine ratio which was closest to the index date. Serum calcium, phosphorus, and creatinine values were obtained within 3 months prior to the biopsy date.

Outcome Variables

Our primary outcome of interest was time in days to ESRD (censored for death). Secondary outcomes were the slope of eGFR from the time of biopsy to 1 year of follow-up and change in AKIN stage [12]. As dialysis dependence was not consistently extracted by INPC methods, the ESRD outcome was defined as a sustained eGFR ≤10 mL/min/1.73 m2, i.e., a mean eGFR <10 mL/min/1.73 m2 in two consecutive 3-month periods of follow-up. Time to ESRD was calculated as days from the date of the biopsy to the first date of the sustained eGFR ≤10 mL/min/1.73 m2. The use of this sustained low eGFR as an ESRD surrogate allowed us to differentiate an episode of AKI from persistent progression to ESRD. Death was ascertained from INPC records and the social security death database.

Statistical Analyses

The index date was defined as the date of the kidney biopsy. Data were described as mean ± standard deviation or median and 25th to 75th percentile (interquartile) range. Peak laboratory tests were identified as the highest value in the 3 months prior to the kidney biopsy. For the cross-sectional comparisons of categorical variables, Fisher’s exact test (two-sided test) was used to compare across different calcification groups. For the continuous variables, two-sample Wilcoxon Rank Sum test (two-sided test) was conducted to test differences between groups. For the survival analysis, we used Cox proportional hazard model in both univariate and multivariate analyses. In multivariate analyses, we included diabetes status, age, and eGFR as covariates. To keep the effects of eGFR proportional over time, we used a split time model (split at 6 months and 2 years of follow-up) in the multivariate Cox proportional hazard analysis. For baseline to 1-year follow-up slope of eGFR analysis, we used linear regression model with the slope as the outcome variable.

Study Population

Of 4,364 biopsy specimens indexed in the database between 2005 and 2017, 428 (9.8%) contained the word “calcification” in native kidney biopsy pathology reports, with approximately 25% of those with calcification showing CaOx deposition. Table 1 describes the demographics, clinical parameters, and biochemical values for these patients as well as the pathologic characteristics of their specimens. Compared to patients without calcification, patients with any form of calcification on kidney biopsy were older, had more comorbidities (congestive heart failure, PVD, DM, HTN, CAD, and tobacco use), and lower eGFR. Patients with CaOx calcification alone, compared to patients with DC or mixed calcification, had fewer comorbidities but were more likely to have history of gastric bypass or malabsorption and take vitamin D. There was no difference in proteinuria between patients with calcifications of any type and those without. In patients with any calcification, the average serum calcium was lower, and peak phosphorus was higher than those without calcification. In the patients who had biopsy specimens showing calcification, the mean calcium was significantly higher in the presence of DC than CaOx only calcification.

Table 1.

Demographics, comorbidities, and laboratory values

Demographics, comorbidities, and laboratory values
Demographics, comorbidities, and laboratory values

Histopathologic Findings

The pathologic findings from each group of kidney biopsy specimens are shown in Table 2. Compared to patients with no calcifications, those with any form of calcification were more likely to have hyaline arteriosclerosis, interstitial fibrosis and tubular atrophy, glomerular obsolescence, and nodular mesangial sclerosis. Those patients with calcifications were also more likely to have a primary pathologic diagnosis of acute tubular injury or acute tubular necrosis when compared to patients without calcification.

Table 2.

Kidney biopsy pathologic findings

Kidney biopsy pathologic findings
Kidney biopsy pathologic findings

Longitudinal Outcomes in Patients with Kidney Biopsy Specimens Demonstrating Calcification

In a median follow-up of 485 days (range 186-1,825), 625 (23.0%) individuals reached the primary outcome of time to ESRD censored for death. As expected, by univariate analysis (online suppl. Table 1; for all online suppl. material, see www.karger.com/doi/10.1159/000525647), increased age, non-white race, higher proteinuria, lower eGFR, heart failure, peripheral vascular disease, DM, HTN, CAD, and smoking all significantly increased the primary outcome. Similarly, more severe histopathologic findings of hyaline arteriolosclerosis, interstitial fibrosis and tubular atrophy, nodules, and glomerulosclerosis decreased time to ESRD censored for death. The presence of any calcification was not significantly associated with time to ESRD censored for death (HR 1.03; 0.69–1.55, p = 0.87). By multivariate analyses including calcification into the model, any calcification (HR 0.59, 0.38–0.92, p = 0.02), higher eGFR (HR 0.76, 0.73–0.79, p < 0.001), and higher age (HR 0.99, 0.98–0.99, p < 0.001) were associated with decreased likelihood of progressing to ESRD. In contrast, a diagnosis of diabetes was associated with greater risk of progression to ESRD (HR 1.94, 1.56–2.42, p < 0.001). We then examined the impact of the presence of any calcification on the progression to ESRD in patients with DM and HTN (Fig. 1), and again demonstrated the presence of any calcification reduced the HR of time to ESRD.

Fig. 1.

The presence of calcification is associated with a reduced eGFR 6 months after kidney biopsy, even in patients with diagnoses of HTN and diabetes.

Fig. 1.

The presence of calcification is associated with a reduced eGFR 6 months after kidney biopsy, even in patients with diagnoses of HTN and diabetes.

Close modal

We then examined factors related to the change in slope of eGFR in the 1 year following kidney biopsy. By univariate analyses (Table 3), non-white race, male sex, peripheral vascular disease, HTN, CAD, proteinuria, lower baseline eGFR, and greater severity of histopathologic features were associated with a greater decline (negative slope/beta) in eGFR. In contrast, and consistent with the results for progression to dialysis, the presence of calcification was associated with a reduced decline in eGFR (beta 0.40) with an r-square in the range of known important biopsy predictors of progressive disease. By multivariate analyses (Table 4), many factors remained significant, and the improvement, or reduction, in eGFR decline in the presence of calcification was stronger. These results suggest that the presence of any calcification was associated with reduced progression to ESRD. We hypothesized this reduced progression may reflect kidney injury recovery from AKI.

Table 3.

Univariate predictors of slope of change in eGFR the first year after biopsy

Univariate predictors of slope of change in eGFR the first year after biopsy
Univariate predictors of slope of change in eGFR the first year after biopsy
Table 4.

Effect of calcification on change in eGFR slope from time of biopsy to 1-year follow-up multivariate analyses

Effect of calcification on change in eGFR slope from time of biopsy to 1-year follow-up multivariate analyses
Effect of calcification on change in eGFR slope from time of biopsy to 1-year follow-up multivariate analyses

To test this hypothesis, we examined the association of AKI and AKI recovery (assessed by AKIN stage change) with calcification. There was more AKI in patients with calcification versus without calcification (48% vs. 30% p < 0.001), and more severe AKI in patients with calcification on biopsy (48%, 15%, 37% stages 3, 2, 1) versus (33%, 13%, 55% stages 3, 2, 1) without calcification. There was also more AKI in the CaOx group than in the DC calcification group (66% vs. 40%, p < 0.001). We then evaluated the percent of patients whose AKIN stage did not change over 1 year, those that worsened, and those that had an improvement in AKIN stage (Fig. 2). In total, there were 858 participants who had AKI without any calcification, 108 participants with calcification. There was significantly greater improvement in AKIN stage in those with calcification versus those without (41.9 vs. 23.9%, p < 0.001) and a trend toward improvement in CaOX versus those with DC calcifications (53.1 vs. 36.1%, p = 0.06).

Fig. 2.

The color distribution indicates the outcome of the AKIN stage at the time of kidney biopsy.

Fig. 2.

The color distribution indicates the outcome of the AKIN stage at the time of kidney biopsy.

Close modal

The results of this large series of nearly 4,000 clinical biopsy specimens demonstrate that calcification was reported in 9.8% of specimens, and approximately 25% of the calcification deposits were identified as CaOx crystals. To our knowledge, this represents the largest collection of nontransplant kidney biopsies evaluated for the consequences of calcification. Patients with any calcification were older, had more comorbidities, a lower eGFR, and more likely to have acute tubular injury/necrosis on biopsy examination. In those patients with only CaOx deposition, there were fewer comorbidities but a history of gastric bypass and vitamin D use. Importantly, the presence of any calcification on kidney biopsy, compared to no calcification, was indicative of slower decline in eGFR slope and reduced risk of progression to ESRD. This lower eGFR at the time of biopsy of kidneys with any calcification, yet slower decline in eGFR and less progression, is consistent with our finding of greater AKI, and presumably, greater recovery of renal function following AKI. Thus, calcification appears to coincide with AKI more than underlying progressive CKD or glomerular disease. Given that a kidney biopsy specimen is not routinely obtained for AKI unless no cause can be identified, we suspect the prevalence of calcifications in the kidney may even be greater. Under-reporting of calcium deposits is multifactorial and may be due to dissolution of crystals (e.g., due to transport solutions, processing techniques, and staining methods); under-recognition of transparent CaOx crystals in nonpolarized tissue sections; lack of consensus reporting criteria; and pathologists’ subjectivity, experience, or perceived relevance of deposits.

The pathogenesis of calcification in the renal tubules is not fully understood. Presumptions are that hypercalciuria is a risk factor for tubular calcification in the form of calcium phosphate and that hyperoxaluria is the primary risk factor for CaOx deposition, similar to the pathogenesis of nephrolithiasis [6]. However, studies in patients with small bowel resection and malabsorption leading to hyperoxaluria have CaOx deposits in the inner medullary collecting ducts [13], but no such depositions are found in specimens from idiopathic CaOx stone formers [14]. This suggests that kidney deposition is not due only to urine concentration of oxalate or supersaturation of CaOx. Whether calcifications induce tubular injury or tubular injury predisposes to calcification is also unknown. However, a recent study demonstrated that CaOx crystals in renal tubules of animals with polycystic kidneys induced tubular dilatation by rapid and persistent activation of mTOR and STAT3 signaling, suggesting the tubular crystals may provide an initial “hit” for cyst formation [15]. This suggests that crystals within the tubular lumen may also activate other pathways leading to renal epithelial damage and as such cause tubular injury/AKI, as compared to the-long held belief that calcification in the renal tubules is a consequence of tubular injury. If this were true, then preventing crystalluria with reduction of calcium and oxalate excretion could be of benefit in preventing some cases of AKI. Thus, avoidance of excess oxalate intake, vitamin C (that is converted to oxalate), or excess calcium/vitamin D intake, especially in the setting of volume depletion may cause or contribute to the severity of AKI. However, prospective studies would be required to confirm causation.

In contrast to our observations of calcification being associated with slower decline in eGFR (due likely to recoverable AKI) in nontransplanted kidneys, the finding of calcification in kidney transplant allograft biopsy specimens conveys poor prognosis and has been well-characterized by several studies. The prevalence of calcium deposition, especially CaOx deposition, varies widely in reports from 4% in a series of 315 biopsies in Texas [16], 9% in a series of 680 patients in Baltimore [17], 19.4% in 346 biopsies in Boston [18], and 53% in a study in Brazil [19]. The higher prevalence in the latter study may reflect an earlier time point of biopsy. All of these studies identified worse graft survival in the presence of CaOx deposition. Palsson et al. [18] recently characterized long-term follow-up and found that CaOx deposition increased delayed graft function by 11.3-fold (CI 6.0–21.4) by multivariate analyses. Additional risk factors included longer time on dialysis [18, 20]. The duration of dialysis prior to transplant may be critical as oxalate accumulates in soft tissue and is elevated in the blood of patients on dialysis, with rapid clearance with a new functioning kidney [21]. Thus, careful attention to urine oxalate and calcium levels in patients with new allografts may be indicated in patients with a long dialysis vintage.

There are several limitations to our study. First, the true prevalence of calcification on kidney biopsies cannot be determined as there is an inherent bias as to who receives a kidney biopsy. Second, this is a single-site study, and prevalence and outcomes may differ by region, especially given differences in dietary risk factors for both hypercalciuria (high sodium, high animal diet) and hyperoxaluria (diet, supplements, and gastric bypass for obesity). Third, the indication for the kidney biopsy was not able to be ascertained as it was often missing from the pathology report and not a variable that was recorded in the EHR. Fourth, despite over 4,000 biopsies, we were underpowered to compare the outcomes of dialysis or death between CaOx and calcium phosphate deposition and thus could only compare presence or absence of calcification for these end points. Further, there may have been individuals with low eGFR who were not on dialysis. However, the strengths include the size of our database, the reading of over 95% of specimens by the same pathologist, and the unique ability to connect to a statewide patient care clinical informatics network to track outcomes longitudinally.

In summary, calcification affects 10% of nontransplant biopsy specimens in our series of 4,000 patients and is associated with AKI more than chronic fibrosis or glomerulonephritis. The presence of calcification conveys an improved prognosis, likely relating the increased association of recoverable AKI, in contrast to worse prognosis in kidney allograft biopsy specimens. The clinical comorbidities for CaOx versus calcium phosphate deposition differ, suggesting that clinical and laboratory evaluation for AKI should also include identification of factors leading to hypercalciuria (idiopathic/stone formation, loop diuretics, hypercalcemia) or hyperoxaluria (diet, supplements, and gastric bypass/malabsorption), and in undiagnosed AKI with such risk factors, a kidney biopsy should be considered to confirm crystal deposition.

This study protocol was reviewed and approved by the Indiana University Institutional Review Board (1601431846), with waiver of informed consent and authorization due to the retrospective nature of the study.

There are no disclosures relevant to this study.

The study was supported from institutional funding. Salary support for authors was provided in part by NIH grants UL1TR002529 (SMM), K23DK102824 (RNM), K08DK107864 (MTE).

Conceived: Sharon Moe, Ranjani Moorthi, and Carrie Phillips; collected and/or analyzed data: Anna Gaddy, Carrie Philips, Michael Eadon, Tae-Hwi Schwantes-An, Ranjani Moorthi, and Sharon Moe; drafted manuscript: Anna Gaddy and Sharon Moe; reviewed and edited paper: all authors.

The information in this manuscript is not public due to containing information that could compromise the privacy of research participants but are available from the corresponding author (S.M.M.) by emailing smoe@iu.edu.

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