Value of “Active” Urine Sediment Examination in Predicting Proliferative Glomerular Pathology on Kidney Biopsy

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Abstract

Key Points

• A good urine sediment examination corelated with clinical history can predict whether the patient has a glomerular or tubular pathology.

• Increase in dysmorphic red blood cells and other formed elements in urine sediment correlates with degree of proliferation in kidney biopsy.

• Active urine sediments are indicative of a proliferative glomerular pathology and inactive urine sediments are indicative of a non-proliferative glomerular pathology.

Background

Urine sediment examination is an important preliminary investigation for the nephrologist and helps them decide whether the patient has a proliferative or nonproliferative glomerular pathology. Recently, there is an increasing trend of using easier, nonspecific dipstick method for urine examination leading to a decline in the importance of urine sediment examination. Here, we attempt to define guidelines for biochemical and microscopic parameters to develop a uniform and clinically relevant reporting system for urine sediment examination.

Methods

Urine samples were reported as inactive or active sediment. A tiered system of reporting urine sediments was developed including inactive sediment, inactive sediment with moderate/significant proteinuria, glomerular hematuria, and active sediment, active sediment with significant proteinuria/features of proliferative activity. The urine sediment was compared with kidney biopsies of these patients, which were grouped into nonproliferative and proliferative glomerulopathy.

Results

Seven hundred and ninety-five paired samples of urine sediment and kidney biopsies were examined and compared. Patients of nonproliferative glomerulopathy (minimal change disease, FSGS, amyloid and membranous nephropathy) showed features of inactive sediment. Patients with proliferative glomerulopathy (focal proliferative GN, diffuse proliferative GN, membranoproliferative GN, mesangio-proliferative GN, and crescentic GN) predominantly showed active sediment, with increase in percentage of dysmorphic red blood cells and formed elements. The sensitivity of this urine reporting system was 82.0%, specificity 74.4% with P value <0.001.

Conclusions

This system of reporting urine sediment is a sensitive and efficient method for predicting the severity of underlying kidney disease and need for performing renal biopsy.

Introduction

Urine sediment examination is one of the most preliminary laboratory tests that is requested in any patient presenting with a suspected kidney disorder.^1,2 The results of the urinalysis in conjunction with the clinical presentation of the patient help the nephrologist to decide whether the patient has a proliferative or nonproliferative glomerular pathology and plan further line of diagnostic tests and treatment.

Recently, there has been an increasing trend of using simpler faster methods such as dipstick method for urinalysis. It is often performed by a technical supervisor who is not sensitized to the requirements of the nephrologist and lacks the clinical understanding to make a clinicopathologic correlation.^3,4 There is lack of specific guidelines and definitions for the assessment of biochemical and microscopic abnormalities in the urine sediment. This has resulted in a decline in the popularity and usefulness of the art of urine sediment examination.

We attempted this study to emphasize that urine sediment examination, when performed by a nephropathologist who is sensitized to the needs of the nephrologist, is an extremely useful and vital test. We have tried to define guidelines and definitions for examined biochemical and microscopic parameters to develop a uniform and clinically relevant reporting system for urine sediment examination. We examined the efficacy of this system by comparing with kidney biopsy findings performed subsequently in these patients to determine the efficacy of this system of urine sediment examination for predicting the requirement of kidney biopsy and clinical follow-up of these patients.

Methods

This study was conducted prospectively on all patients admitted to the departments of Medicine and Pediatrics in Maulana Azad Medical College and associated GB Pant Hospital, New Delhi, for various nephrologic complaints. A midstream second morning urine sample was collected in a sterile container after hygienically cleaning the external genitalia. The urine sample was received in a specialized laboratory for urine sediment examination in the nephropathology laboratory of our hospital along with a brief clinical history. All cases where the urine microscopic findings were indicative of a stale, ill-preserved sample were excluded from the study.

Processing of Urine Samples

The urine samples were processed within 1 hour. Physical examination included color, turbidity, and pH. Ten millilitres of urine was centrifuged at 2000 rpm for 10 minutes at room temperature. The supernatant was tested for sugar using dipstick method and semiquantitative protein estimation using sulpho-salicylic precipitation method.⁵ The protein was graded from 1+ to 4+, as per established criteria.⁶ Proteinuria was classified as moderate if 2+ and significant if 3+ or more.

For the microscopic examination, the urinary precipitate was resuspended in 1 ml of supernatant urine. One drop of supravital stain (3% crystal violet [colour index 42555] and 0.25% sarfranin O [colour index 50240] mixed in 1:10 ratio and containing a few ml of ethanol) was added to stain the cellular components. This stain allows easy recognition of formed cell elements in the urine sediment under bright field microscopy, negating the use of a phase contrast microscope.^7,8 It helps in the preservation of the formed cell components by the ethanol it contains so that the sediment can be kept in the refrigerator and examined at will.

Microscopic Examination of Urine

The urine sediment examination was examined by two experienced nephropathologists with 20 years and 2 years training in renal pathology, respectively. One drop of the prepared supernatant was examined under the 22×22-mm cover slip. The number and nature of casts was assessed under low power (100× magnification). The number of red blood cells (RBCs), white blood cells (WBCs), epithelial cells, crystals, and fat bodies were noted under high power (400× magnification). The presence of RBCs and WBCs more than five per high power field (HPF) was regarded as abnormal.

The morphology of RBCs was carefully examined under high power. Dehemoglobinized RBCs with irregular crenated outlines (Figure 1, A–H) were regarded as dysmorphic with a glomerular origin. If more than 20% of the RBCs were dysmorphic, the hematuria was labeled as “glomerular hematuria.”^9–13 The presence of acanthocytes (G1 cells; Figure 1, A–G) with cytoplasmic blebs was regarded as highly significant for glomerular hematuria.^14–17 The findings of urine sediment examination were subsequently compared with the kidney biopsy findings which was submitted in due course of time as part of routine diagnostic examination.

Figure 1.

Microphotograph showing microscopic features of active sediment in urine. (A–H) Morphology of dysmorphic RBCs in wet preparation of urine showing RBCs with irregular loss of hemoglobin, irregular outlines and blebs; G1 cells are identified in (A–G) and labeled with arrow in (B; 600× magnification); (I) microphotograph showing features of active sediment including dysmorphic RBCs and WBCs+(magnification 200×); (J) active sediment with features of proliferation showing the presence of WBC cast (magnification 400×). RBC, red blood cell; WBC, white blood cell.

Developing a Standard System of Reporting Urine Sediment for the Nephrologist

The currently used method of microscopic urine examination of urine simply states type and number of all formed elements present. To make the urine report more diagnostic and informative, we developed a standardized system of reporting urine sediment (Table 1) giving importance to two aspects: degree of proteinuria and presence of glomerular hematuria. The urine sediment was classified as “inactive” when it did not show features of glomerular hematuria and further subclassified according to the degree of associated proteinuria into the following five subgroups:

1. Inactive sediment alone: when not associated with proteinuria or showing minimal quantities of proteinuria (up to 1+).

2. Inactive sediment with moderate proteinuria (associated with 2+ protein).

3. Inactive sediment with significant proteinuria (associated with 3+ or more protein).

4. Inactive sediment+WBCs (more than 5/HPF) indicative of pyuria.

5. Inactive sediment+WBCs +WBC casts indicative of Interstitial nephritis.

Table 1.

Tiered system of reporting urine sediment

S No.	Urine Sediment Report	Details
1.	Inactive sediment alone	When not associated with proteinuria or showing minimal quantities of proteinuria (up to 1+)
2.	Inactive sediment with moderate proteinuria	Associated with 2+ protein
3.	Inactive sediment with significant proteinuria	Associated with 3+ or more protein
4.	Inactive sediment+WBC	(More than 5/HPF) indicative of pyuria
5.	Inactive sediment+WBCs +WBC casts	Indicative of interstitial nephritis
6.	Glomerular hematuria	RBCs more than 5/HPF, 20% of which are dysmorphic
7.	Active sediment	RBCs more than 5/HPF, 20% of which are dysmorphic Associated with 2+ protein
8.	Active sediment with significant proteinuria	RBCs more than 5/HPF, 20% of which are dysmorphic Associated with 3+ or more protein
9.	Active sediment associated with features of a proliferative glomerulopathy	RBCs more than 5/HPF, 20% of which are dysmorphic Associated with 3+ or more protein or Associated with cellular casts

HPF, high power field; RBC, red blood cell; WBC, white blood cell.

When glomerular hematuria was associated with moderate proteinuria, the sediment was classified as “active sediment” (Figure 1). Associated features such as significant proteinuria were also mentioned in the diagnosis. Active sediment associated with cellular casts such as RBC and WBC casts was regarded as highly significant of a proliferative glomerulopathy (Figure 1J).¹⁸

When the glomerular hematuria was associated with nil or minimal proteinuria (up to 1+), it was reported as “glomerular hematuria” alone. Active sediment was further subclassified into four subgroups.

1. Glomerular hematuria.

2. Active sediment (glomerular hematuria+moderate proteinuria).

3. Active sediment with significant proteinuria (associated with 3+ or more protein).

4. Active sediment associated with features of a proliferative glomerulopathy (glomerular hematuria+moderate proteinuria+cellular casts—RBC cast or WBC cast).

A tubular pathology was suspected on the basis of clinical features and presence of more than five WBCs/HPF which was reported as pyuria (Figure 2A). Associated RBCs, if present, did not show dysmorphic features. Interstitial nephritis was diagnosed when inactive sediment was associated with pyuria and WBC casts (Figure 2B).

Figure 2.

Miscellaneous microphotographs of urine sediment examination. Microphotographs showing (A) the presence of increased WBCs in a case of pyuria (magnification 400×); (B) increased WBCs along with WBC casts in a case of interstitial nephritis (magnification 200×); (C) fresh RBCs in a case of nonglomerular hematuria (magnification 400×); (D) mixed hematuria in a case of IgA nephropathy with both well hemoglobinized fresh RBCs and dysmorphic RBCs (magnification 400×); (E) fresh RBCs showing the presence of Howell Jolly bodies (magnification 600×); (F) fresh RBCs at the edge of the cover slip showing artifactual changes resembling dysmorphic RBCs (magnification 400× with inset at magnification 100×).

Nonglomerular hematuria was diagnosed when more than 90% of the RBCs in the urine sediment showed a normal morphology with good hemoglobinization (Figure 2C) and was identified in cases of renal stones, high-grade fever, pyelonephritis, and vascular disorders.⁵

Mixed hematuria was diagnosed when a dual population of hemoglobinized and dysmorphic RBCs was identified (Figure 2D). Although the percentage of dysmorphic RBCs was <20%, a comment on their presence was included in the urine sediment report. Such a finding was identified in urine sediments examined postkidney biopsy or in patients of IgA nephropathy.

The presence of lipid casts and fat bodies in association with proteinuria was indicative of lipiduria in patients of nephrotic syndrome (Figure 3D). Other casts such as granular, hyaline, and tubular epithelial casts were not of significant diagnostic importance (Figure 3, B, C, and E, respectively).

Figure 3.

Miscellaneous microphotographs of urine sediment examination. Microphotographs showing (A) epithelial cells, (B) coarse granular casts, (C) broad hyaline cast, (D) lipid cast, (E) WBC cast, and (F) Bile casts in a case of bile cast nephropathy (magnification 400×).

Correlation of Activity of the Urine Sediment with the Kidney Biopsy

The above-described system of urine sediment reporting was subsequently compared with the kidney biopsy findings which was later received in our laboratory to examine its efficacy in predicting possible kidney biopsy diagnosis. We developed this system of urine sediment examination to indicate to the nephrologist whether his patient was suffering from a glomerular pathology and indicate the degree of proliferative activity. The glomerular involvement being an indicator for renal biopsy helped to plan further treatment protocol.

We hypothesized that inactive sediment with varying degrees of proteinuria may be expected in minimal change disease (MCD), FSGS, membranous nephropathy (MN), and amyloidosis.

Similarly, we expected that active sediment with or without proliferation may be seen in focal proliferative GN, diffuse proliferative GN (DPGN), mesangioproliferative GN (MesGN), membrano-proliferative GN (MPGN), and crescentic GN (CGN).

To verify this system of urine sediment reporting, the urine report was compared with the kidney biopsy findings which was performed subsequently. The kidney biopsy diagnosis was confirmed on light microscopy (LM) and immunofluorescence (IF). The sample for LM was processed as per routine methods and stained with hematoxylin and eosin and special stains such as periodic acid-Schiff, Jones silver methenamine, and Mason trichrome stain.

For IF, the biopsy was received in Michel medium. 3-μm thick frozen sections were cut and stained with various immunoglobulins conjugated with FITC. These included γ (IgG), μ (IgM), α (IgA), complements (C3, C1q), fibrinogen, and kappa and lambda light chains. Electron microscopy was also performed when sample was available and findings correlated with clinical history and LM findings.

Statistical Analysis

Statistical analysis was performed using the paired t test for within-group and the unpaired t test for between-group comparisons. Wilcoxon rank-sum and signed rank tests were applied when required. All data were analyzed using the SPSS version 28. The chi-square test was applied to study the significant association between the groups. The criterion for statistical significance was P < 0.05 or less.

Statistical analysis included comparison of degree of proteinuria, presence of dysmorphic RBCs, and other formed elements (RBC and WBC casts) in urine with the kidney biopsy diagnosis, which was regarded as gold standard for purpose of analysis. Specifically, we compared the urine sediment diagnosis according to the tiered classification, with the final kidney biopsy diagnosis on LM and IF.

Results

A total of 922 paired samples of urine and kidney biopsy were received in the renal pathology laboratory of the Department of Pathology, GB Pant Hospital, over a period of 15 years (2008–2023). Of these, 114 were excluded from the study when the accompanying kidney biopsy was found to be inadequate, or a diagnosis of chronic GN, cortical infarct, diabetic nephropathy, and hypertensive nephropathy was made as most of these biopsies showed severe chronic parenchymal damage and urine sediment examination showed significant proteinuria without reflecting on the glomerular pathology. A total of 795 cases were thus included in the final analysis. Figure 4 is a flow diagram illustrating the sequence of events as above.

Figure 4.

Flow diagram showing analysis of urine sediment (inactive versus active) compared with kidney biopsy diagnosis.

The age of these patients ranged from 1 year to 70 years with a mean of 23 years. Of these, 384 were men and 411 women with a male:female ratio of 0.93:1. The kidney biopsy of these patients was grouped in two groups:

1. Nonproliferative GN including MCD, FSGS, MN, and amyloid.

2. Proliferative GN including focal proliferative GN, DPGN, MesGN, MPGN, and CGN.

Breakup of kidney biopsies is presented in Table 2. The urine sediments were examined by the above-described method and classified according to the tiered system into “inactive” or “active” as the case may be, as presented in Table 1. A comparative chart of nature of urine sediment and associated kidney biopsy findings is prepared and presented in Table 3.

Table 2.

Total number of cases in each kidney biopsy group

Kidney Biopsy Diagnosis	No of Cases (N)	Percentage (%)
Nonproliferative group
MCD	233	48.64
FSGS	95	19.83
MGN	94	19.62
Amyloid	57	11.89
Proliferative group
Mes PGN	66	20.88
DPGN	118	37.34
MPGN	67	21.20
CGN	36	11.39
Focal proliferative GN	29	9.17
Total	795

CGN, crescentic GN; DPGN, diffuse proliferative GN; MCD, minimal change disease; Mes PGN, mesangioproliferative GN; MGN, membranous GN; MPGN, membranoproliferative GN.

Table 3.

Urine sediment findings in different kidney biopsy groups

	Kidney Biopsy Report
Urine Report	MCD	FSGS	MGN	Amyloid	Mes PGN	DPGN	MPGN	CGN	FPGN	Total
IS	90	14	21	10	0	4	6	2	6	153
IS-MP	40	22	14	11	8	5	8	3	3	114
IS-SP	75	31	32	33	13	7	12	1	3	207
GH	2	0	0	0	15	12	4	0	4	37
AS	4	7	2	0	12	22	11	8	5	71
AS-SP	10	11	8	2	10	43	15	19	2	120
AS-PF	1	1	0	0	4	22	7	2	2	39
MILD-AS	11	9	17	1	4	3	4	1	4	54
Total	233	95	94	57	66	118	67	36	29	795

AS, active sediment; AS-PF, active sediment with proliferative features; AS-SP, active sediment with significant proteinuria; CGN, crescentic GN; DPGN, diffuse proliferative GN; FPGN, focal proliferative GN; GH, glomerular hematuria; IS, inactive sediment; IS-MP, inactive sediment with moderate proteinuria; IS-SP, inactive sediment with significant proteinuria; MCD, minimal change disease; Mes PGN, mesangioproliferative GN; MGN, membranous GN; MILD-AS, mildly active sediment; MPGN; membranoproliferative GN.

Patients of MCD (n=233) as predicted showed features of inactive sediment with varying degrees of proteinuria (n=205; 87.98%) depending on the efficacy of treatment. Proteinuria ranged from nil to 1+ in patients who showed remission on steroids to significant in those patients who were freshly diagnosed or resistant to steroid therapy. The urine samples thus helped in the follow-up of these patients in regard to efficacy of management. Similar results were also obtained for 67 patients of FSGS (n=95; 70.52%). The presence of inactive sediment in patients of MCD and FSGS was found to be statistically significant with a P value of < 0.001. Fifty-four patients of amyloidosis also showed inactive sediment with significant proteinuria out of 57 cases (94.73%; P=0.001).

Most patients with MN (67/94) presented with inactive sediment with proteinuria (71.27%). About 18% of these patients (n=17) presented with significant proteinuria with mild glomerular hematuria (about 8–10 RBCs/HPF, most of which showed dysmorphic changes). Such sediments were reported out as mildly active sediment with significant proteinuria.

Patients with proliferative GN (focal proliferative, DPGN, MPGN, MesGN, and CGN) presented with glomerular hematuria with variable levels of proteinuria indicative of the proliferative nature of the lesion. Depending on the degree of proliferation, the urine sediment showed increased number of cellular components including RBCs, WBCs, and cellular casts. There was a significant difference of dysmorphic RBCs and cellular components between the proliferative and nonproliferative group of GN (P < 0.001; Table 4 and Supplemental Tables 1–3). The percentage of dysmorphic RBCs increased exponentially with the proliferative activity (P < 0.001; Figure 5 and Supplemental Table 1). When the active sediment was associated with RBC and WBC casts, it was indicative of a greater proliferative activity in the renal biopsy amounting to a diffuse proliferative lesion (Supplemental Tables 2 and 3).

Table 4.

Comparison of urine sediment findings with nonproliferative and proliferative GN

Kidney Biopsy	Urine Sediment		Total	P Value
	Inactive Sediment	Active Sediment
Non proliferative GN	393 (82.91%)	86 (26.79%)	479	0.001
Proliferative GN	81 (17.08%)	235 (73.20%)	316
Total	474	321	795

Figure 5.

Bar diagram showing trend of dysmorphic RBCs in different kidney biopsy groups. CGN, crescentic GN; DPGN, diffuse proliferative GN; FPGN, focal proliferative GN; MCD, minimal change disease; MESPGN, mesangioproliferative GN; MGN, membranous GN; MPGN; membranoproliferative GN.

Patients of SLE (n=130) included in the study were grouped according to the International Society of Nephrology/ Renal Pathology Society system of classification and then included in the morphologic subgroups of kidney biopsy (nonproliferative or proliferative). Their urine samples were accordingly analyzed. They were also found to correlate with this system of reporting. The urine sediment examination could be developed into a system of follow-up in these patients in regard to the efficacy of immunosuppression and development of flares.

The sensitivity and specificity of tiered system of urine sediment examination to predict kidney biopsy as proliferative of nonproliferative pathology were examined keeping the kidney biopsy diagnosis as the gold standard. The sensitivity of urine reporting system was found to be 82.0%, and specificity was 74.4% with a P value of <0.001. The positive predictive value of this system of urine sediment analysis was 82.9% with a negative predictive value of 73.2%. Thus, this system of reporting urine sediment is a sensitive and efficient method of predicting the severity of the underlying kidney disease and need for performing renal biopsy.

Discussion

The tiered system of urine sediment examination is a clinically relevant system of reporting urine. It attempts to correlate the clinical presentation of the patient with biochemical and microscopic features in the urine sediment. It helps the nephrologist to decide whether the patient is suffering from an active glomerular pathology requiring a kidney biopsy. In patients with inactive sediment, the degree of proteinuria helps the nephrologist to assess the efficacy of immunosuppressive therapy. This differentiation is important as performance of the renal biopsy is an invasive procedure often laden with risks for the patient.

Differentiation between isomorphic and dysmorphic erythrocytes is extremely important in the analysis of the urine sediment. Isomorphic RBCs (Figure 3A) possess a biconcave shape with a central pallor and smooth edges accounting for approximately half of the RBC diameter. They may be seen in extraglomerular diseases such as interstitial nephritis, nephrolithiasis, urinary tract infections, and urothelial malignancies.¹⁹ RBCs and RBC casts can also appear after vigorous exercise.

Dysmorphic RBCs exhibit irregular central pallor with uneven edges or a distinct target-like appearance. They may at times show a ring shape with single or multiple blebs or protrusions.²⁰ They are most likely caused by mechanical damage while passing through the damaged glomerular basement membrane and proliferating endothelial cells. Further damage is inculcated by osmotic injury during passage through hypotonic tubular fluid and chemical factors such as change in pH.^21–23 This results in loss of basement membrane material and smaller size (approximately 3 μm).

One of the important diagnostic criteria used in this study was the cutoff figure of 20% dysmorphic RBCs as an indicator of glomerular hematuria. This has been recommended by previous studies and also applied in our study.⁷ Other studies have, however, recommended cutoffs varying from 15%⁸ to 35%.¹ The percentage of dysmorphic red cells also tends to vary with progression of disease. Thus, in patients with borderline percentage of dysmorphic red cells, it is advised to examine the urine sediment on at least two occasions to better decide the renal pathology.

Correlation of urine microscopic examination with kidney biopsy findings has only been attempted in a few publications over the years.^24–26 Our findings correlate with other studies which have also shown that the percentage of dysmorphic RBCs and cellular casts are the most important features in predicting the presence of a proliferative glomerulopathy.^21,24 This system of urine sediment examination was useful in differentiating between proliferative and nonproliferative lupus nephritis. Similar results were obtained in previous studies by Gamaleldin et al.²⁷

It is also a useful follow-up tool especially in patients of proliferative GN such as diffuse lupus nephritis, DPGN, or MPGN. A decrease in the proteinuria of the percentage of RBCs, WBCs, or cellular casts heralded a good response to therapy. By contrast, an active sediment in a patient of SLE Class 2/Class 5 often signified a flare and an indication that increased immunosuppression, or a kidney biopsy was required.

It can be challenging to differentiate acanthocytes from pseudo-G1 cells (echinocytes, stomatocytes, schistocytes, sickled cells, poikilocytes, etc.). Pseudo-G1 erythrocytes may become crenated in concentrated urine. Red cells exposed in vitro to a hemolytic environment may resemble acanthocytes (Figure 2F).²¹ However, they are well hemoglobinized and often show inclusions of precipitated ribosomal ribonucleic acids as seen in reticulocytes which are stained by the vital stains in the dye, an indicator toward the diagnosis (Figure 2E).

It is imperative to process the urine sample within 1 hour, especially in hot conditions of tropical countries where the cells undergo a rapid degeneration. Proliferation of bacteria also leads to a change in the pH further disturbing the morphology. Drying the urine sediment preparation at the edge of the cover slip often leads to crenation of RBCs and an erroneous diagnosis of glomerular hematuria (Figure 3F, inset).

In conclusion, this tiered system of urine sediment examination, when well correlated with the clinical history and performed by a nephropathologist, is an important preliminary diagnostic investigation in any nephrology set up. It is a sensitive and specific diagnostic tool which points the diagnosis toward a proliferative glomerulopathy, an important indicator for a kidney biopsy.

Supplementary Material

kidney360-7-335-s001.pdf ^{(2.6MB, pdf)}

kidney360-7-335-s002.pdf ^{(129.9KB, pdf)}

Disclosures

Disclosure forms, as provided by each author, are available with the online version of the article at http://links.lww.com/KN9/B241.

Author Contributions

Conceptualization: Vineeta V. Batra.

Data curation: Aakash Batra, Vineeta V. Batra, Niharika Jain.

Formal analysis: Vineeta V. Batra.

Investigation: Mukta Mantan, Abhijeet Saha.

Writing – original draft: Vineeta V. Batra, Aarti Verma.

Funding

None.

Data Availability Statements

Original data generated for the study will be made available on reasonable request to the corresponding author. Aggregated Data.

Supplemental Material

This article contains the following supplemental material online at http://links.lww.com/KN9/B242.

Supplemental Table 1. Percentage of dysmorphic RBCs in urine of different kidney biopsy groups.

Supplemental Table 2. Urine cellular components in nonproliferative and proliferative GN; quantitative analysis.

Supplemental Table 3. Percentage of urine particles in different kidney biopsy class.